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Endo/Repro Block1 > Endocrine Path "Bites" > Flashcards

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
Q

What is this a picture of?

A

psammoma body of thyroid [papillary carcinoma]

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26
Q

Tell me about Follicular Thyroid Carcinoma

A
  • 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

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27
Q

What is medullary Thyroid carcinoma

A
  • 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
Q

What is Anaplastic Thyroid carcinoma

A
  • rare
  • F>M, 50s-60s
  • bulky, fast growing, invasive neck mass
  • usually metastatic @ Dx
  • very bad Px [<10% 5y survival]
29
Q

What are the major causes of HyperCa+?

A

MD PIMPS ME

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
Q

MCC of Sx’c hyperCa+?

MCC of aSx’c hyperCa+?

A

Sx’c: malignancy

Asx’c: hyperPT

31
Q

What are the 1’, 2’, 3’ & psuedo causes of hyperPT?

A

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
Q

What are signs/sx’s of 1’ HyperPT?

A

often ASx’c but…

STONE: K stones, and others

BONE: pain, brown tumors, worse [osteoP?]

GROAN: GI problems

MOAN: mental changes

33
Q

Lab findings in 1’ HyperPT?

A

^^Ca+

^^PTH

decreased phosphate

34
Q

What is MCC of 1’ HyperPT?

what genetics may be involved?

A

MCC = PT Adenoma

genetics: PRAD1 overexpression
* MEN1 loss or mutation

35
Q

MCC of 2’ HyperPT?

A

renal failure–> chronic hypoCa

  • can’t excrete phosphate–> ^^PO4
  • excess PO4 –> binds Ca+
  • Ca+ decreases = hypoCa+
  • hypoCa+ –> stims PT’s
36
Q

What are signs and Sx’s of hypoPT?

A
  • •Neuromuscular irritability
    • •Perioral numbness
    • •Muscle weakness, cramps, tetany
    • •Chvostek’s sign
    • •Trousseau’s sign
  • •Heart arrhythmias
  • •Dental abnormalities [enamel hypoplasia]
37
Q

What are the main causes of hypoPT?

A
  • iatrogenic
  • hereditary
    • DiGeorge syn
    • Agenesis [X-linked] of PT’s
  • Idiopathic atrophy
38
Q

What are the major fxns of cortisol?

A

cortisol is BBIIG:

maintains BP

breaks down Bone

suppresses Inflammation

suppresses Immune system

stimulates Gneo

39
Q

What are the the 4 forms of cushing syndrome?

A

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
Q

What is the MCC of Cushing Syndrome?

A

Iatrogenic Cushings! [steroid use]

  • atrophy of adrenal cortex
  • labs: ^^cortisol & decreased ACTH
41
Q

What would you see in pituitary cushings?

  • labs
  • adrenal glands
  • what would happen with a high dose DEX test
A
  • hyperplastic adrenal cortices
  • labs: ^^cortisol
    • ^^ACTH
  • Hi DEX: suppresses cortisol!!!
42
Q

What would you see in adrenal cushings?

  • causes?
  • morph of adrenal
  • labs?
  • dex test?
A

Causes: adenoma, hyperplasia, carcinoma

  • cortex: hypoplastic or hyperplastic
  • labs: ^^cortisol, decreased ACTH

DEX: no suppression!!!

43
Q

What would you see in paraneoplastic cushings?

-cause

labs?

adrenal cortices?

DEX?

A

causes: small cell lung carcinoma secretes ACTH
- adrenal hyperplastic cortices

LABS: ^^cortisol & ^^”fake”ACTH

DEX: no suppression

44
Q

What findings would yuo see in hyperaldosteronism?

A

^^aldosterone: duh

^^BP

hyperNa+

hypoK+

45
Q

1’ hyperaldosteronism causes?

Sx’s?

A
  • ­ ^^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
Q

2’ hyperaldosteronism

-sx’s

common cause/assoc

A
  • ­ ^^renin–> ^^aldosterone
  • Congestive heart failure
  • decreased renal blood flow
  • Renin-producing tumors

**same sx’s & findings as 1’ but with **^^renin **too

47
Q

What should we associate with sudden virilization?

A

adrenocortical tumor

  • rare
  • abd mass
  • necrotic, “ugly” tumor
  • Bad Px
48
Q

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?
A

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
Q

What are causes of 1’ chronic adrenal insufficiency?

MCC?

Sx’s?

A

too little cortisol & mineraloC’s

MCC: autoI–> Addison Disease

Sx’s: weakness, fatigue, GI complaints

  • hypoTN
  • skin hyperpigmented
50
Q

What do we Tx Addison’s Disease with?

A

Tx Sx’s [in crisis]: w/ IV NA+, dextrose, hydrocortisone

Daily after crisis: cortisol & prednisone [carries crisis kit: hydrocortisone]

51
Q

Primary Acute Adrenal Insufficiency

causes?

A

adrenals suddenly aren’t releasing their stuff

causes:

  • addisonian crisis
  • rapid steroid w/drawal
  • massive adrenal hemorrhage
    • WF syndrome
52
Q

What is Waterhouse-Friderichsen Syn?

A

leads to 1’ Acute Adrenal Insufficiency

  • Bacterial infection (N. meningitidis)
  • Hypotension, shock
  • DIC
  • Massive, bilateral adrenal hemorrhage
  • Rapidly progressive
53
Q

WI 2’ adrenal insufficiency?

causes?

findings?

A

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
Q

Pheochromocytoma…WI it?

10%….

what is found in the urine?

A

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
Q

What are the Sx’s of pheochromocytoma?

6 P’s!!!

A
  • Pressure [^^BP]
  • Pain [HA]
  • Perspiration
  • Palpitations [tachyC]
  • Pallor
  • Paroxysms
56
Q

When I say Zellballen, you say…?

A

pheochromocytoma

zellballen= configuration of cells in tumor

57
Q

Where is neuroblastoma derived from?

what gives a better Px?

A

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
Q

What cell types will be in adrenal neuroblastoma biopsy?

A

homer-wright rosettes

59
Q

What characteristics give MEN syndrome WORSE Px?

A

younger

multiple organs

multifocal

aggressive

60
Q

Who is sexy?

Brad Pitt or John Cleecy?

A

John Cleecy!!!

61
Q

Where would you find tumors in MEN 1 vs MEN2?

A

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
Q

What are the 3 P’s of MEN1?

& other!

A

PT hyperplasia: MC manifestation, hyperCa+

Pancreatic endocrine tumors: gastrinoma {ZE syn}, Insulinoma [hypoGly], usually metastatic at Dx, BAD news

PITTuitary adenoma: prolactinoma usually

Other duo gastrinoma, carcinoid, thyroid/adrenal adenomas, lipomas

***brad Pitt is men1

63
Q

What are the genetics associated w/ MEN1?

A

MEN1 gene mutation

[a tumor suppressor gene that encodes menin]

**brad Pitt = men1: run of the mill & turns you off

64
Q

MEN 2A syndrome?

what tumors?

what guy?

A
  • 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
Q

What are the genetics of MEN2A?

A

RET gene mutation

protooncogene

encodes tyrosine kinase R

mutation turns you on!!! like john cleecy

66
Q

Where do you see tumors in MEN2B?

what genetics are involved

A

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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