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06 Endocrine

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0% found this document useful (0 votes)
20 views20 pages

06 Endocrine

Uploaded by

Sanjeev Tanwar
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
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6

Endocrine

Prometheus Lionhart, M.D.

343

ADH_2020
SECTION 1:
ADRENAL

Anatomy: The adrenal glands arc paired retroperitoneal glands that sit on each kidney.
The right gland is triangular in shape, and the left gland tends to be more crescent shaped. If
the kidney is congenitally absent the glands will be more flat, straight, discoid, or ‘‘pancake’’
in appearance. Each gland gets arterial blood from three arteries (superior from the inferior
phrenic, middle from the aorta, and inferior from the renal artery). The venous drainage is via
just one main vein (on the right into the IVC, on the left into the left renal vein).

Zona Glomerulosa

Cortex Zona Fasciculata

Zona Reticularis
Medulla

Step 1 Trivia: There are 4 zones to the adrenal, each of which makes different stuff.

• Zona Glomerulosa: Makes Aldosterone


- prolonged stimulation here leads to hypertrophy.
• Zona Fasciculata: Makes Cortisol
• Zona Reticularis - Makes Androgens
• Medulla - Makes Catecholamines

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Adrenal Ultrasound Cases - Gamesmanship
If you get shown an adrenal case on ultrasound, then you are almost certainly dealing with a
peds case. What that means is that your choices are narrowed down to: (a) normal,
(b) neuroblastoma, (c) hemorrhage, and (d) hyperplasia.

Normal: In babies, the cortex is hypoechoic, and the medulla is hyperechoic. This gives
the adrenal a triple stripe appearance (dark cortex, bright medulla, dark cortex).

Normal Adrenal - Hypoechoic Cortex, Hyperechoic Medulla, Hypoechoic Cortex


- like an Oreo, with a cream filling.

Neuroblastoma:

I talk about this a ton in the peds chapter. To rehash the


important parts, they form in the adrenal medulla
(usually), and typically look like an enlarged gland with
a hyperechoic component. Having said that they can
have cystic components and look like hemorrhage. For
the purpose of multiple choice I'd go with hyperechoic.

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Hemorrhage:

This occurs most commonly in the setting of


trauma or stress (neonates). What this typically
looks like on ultrasound is an enlarged gland with
an anechoic component. With time, the clot
changes and it can be more and more echogenic.
So basically, it can look like anything but for the
purpose of multiple choice I’d go with anechoic.

Second order path type trivia/knowledge:

* Stress: It’s classically seen after a breech birth, but can also be seen with fetal
distress, and congenital syphilis. Imaging features change based on the timing of
hemorrhage. Calcification is often the end result (that could be shown on CT or
MR). It should be avascular. This can occur bilaterally, but favors the right side
(75%).

o Classic Next Step: Serial ultrasounds (or MRI) can differentiate it from a
cystic neuroblastoma. The hemorrhage will get smaller (cancer will not).

o So which is it? Serial ultrasound or MRI? - If forced to pick you want serial
ultrasounds. It’s cheaper and doesn’t require sedation.

• Trauma: This is going to be an adult (in the setting of trauma). Most likely it will be
shown on CT. It’s more common on the right.

• Waterhouse-Friderichsen Syndrome - Hemorrhage of the adrenal in the


setting of fulminant meningitis (from Neisseria Meningitidis).

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Hyperplasia:

What this typically looks like on ultrasound is a “big


adrenal” that “looks like a brain.” So what does "big”
mean? Most sources will say longer than 20 mm, and a
limb that is thicker than 4 mm (although this is debated -
and will likely not be asked). For the purpose of multiple
choice I would say that if they stick calibers on it, then it is
too big. So what does "looks like a brain ” mean? That
means the surface is wrinkled, like it has gyri and sulci. Cerebri form Pattern

Second order path type trivia/knowledge:

• 21-Hydroxylase Deficiency: Congenital adrenal hypertrophy is caused by


21-hydroxylase deficiency in > 90% of cases. It will manifest clinically as either genital
ambiguity (girls) or some salt losing pathology (boys). The salt losing can actually be
life threatening. The look on imaging is adrenal limb width greater than 4 mm. In some
cases you lose the central hyperechoic stripe (the whole thing looks like cortex).

• I say “Genital ambiguity”, you say 21-Hydroxylase Deficiency

• Too much cortisol from overproduction of ACTH - which results in bilateral


adrenal gland hyperplasia. If someone wanted to be a real asshole they could get into the
weeds with vocabulary. For example, the “Disease” vs “Syndrome” THIS vs THAT:

• Cushing Disease: This is an overproduction of ACTH by a pituitary adenoma,


resulting in too much cortisol. This is actually the most common cause of excess
cortisol (75%).

• Cushing Syndrome: The “syndrome” is basically a variety of causes resulting


in common symptoms. So you can have overproduction of ACTH by an ACTH
secreting tumor (classic step 1 example is the small cell lung tumor), or
overproduction of ACTH via an adrenal adenoma (these cases will not have
hyperplasia), or you can have straight up primary adrenal hyperplasia. You could even
get the “syndrome” by taking chronic high dose steroids. Any way you end up with a
fat moon face and big gross lines all over you belly counts as “syndrome.”

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—Summary / Rapid Review—

Normal:

- Triple Stripe
- Hypoechoic Cortex,
- Hyperechoic Medulla,
- Hypoechoic Cortex
- Smooth Surface

Hyperplasia:

- Big (longer than 20 mm)


- Looks like a brain (wrinkled surface)
- Can sometimes lose the central bright layer

- “Genital ambiguity”, = 21-OH Deficiency

Hemorrhage:

- Big with an anechoic (or echogenic) component


- Gets smaller over time

- Seen with “stress” or trauma

Neuroblastoma:

- Big with an echogenic (or anechoic) component


- Does NOT gets smaller over time

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Adrenal Adenoma:
These things are easily the most common tumor in the adrenal gland. Up to 8% of people
have them. Proving it is an adenoma is an annoying (testable) problem.

• Non-Contrast: Less than 10 HU

• Contrast: Two options:

Absolute Washout

Enhanced CT - Delayed CT
________ x 100 Greater than 60% = Adenoma

Enhanced CT - Unenhanced CT

Relative Washout

Enhanced CT - Delayed CT x 100 Greater than 40% = Adenoma

Enhanced CT

• Hypervascular mets (usually renal, less likely HCC) can mimic adenoma washout.
Portal venous HU values > 120 should make you think about a met.

• Along those lines Pheochromocytomas can also exhibit washout. The trick is the same,
if you are getting HU measurements > 120 on arterial or portal venous phase you can
NOT call the thing an adenoma.

• MRI: Look for drop out on in and out of phase T1.

Adrenal Adenoma -Signal drop out in and Out of Phase

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Adrenal Adenoma Continued
• Real Life = Mass in Adrenal = Adenoma

• Multiple Choice = Mass in the Adrenal = Possible Fuckery

• Although most adenomas are not functional, Cushings (too much cortisol) and Conn’s (too
much aldosterone) can present as functional adenoma.

Tips / Tricks:

• Adenoma are usually homogeneous. If they are showing you hemorrhage (in the absence of
trauma), calcifications, or necrosis you should start thinking about other things.
• Adenomas are usually small (less than 3 cm). The bigger the mass, the more likely it is to
be a cancer. How big? Most people will say more than 4 cm = 70% chance cancer, and
more than 6 cm = 85% chance cancer. The exceptions are bulk fat (myelolipomas) or
biochemical catecholamines in the question stem (pheo) - those can be big.
• Bilateral Small = Probably adenoma
• Bilateral Large = Pheo or Met (Lung cancer)
• Portal Venous Phase HU > 120 = Probably a met (RCC, HCC) or pheo.

“Collision Tumors” - Two different tumors that smash together to look like one mass.
Usually one of them is an adenoma. Remember adenoma should be homogenous and small.
If you see heterogenous morphology consider that you could have two tumors. FDG PET
and MRI can both usually tell if the tumor is actually a collision of two different tumors -
those would be the appropriate next steps.

Conn’s Syndrome - Syndrome of excessive aldosterone production. This is most


commonly caused by a benign adenoma (70%). Cortical-carcinoma can also do it, but that
is much more rare and usually accompanied by hypercortisolism.

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Pheochromocytoma
Uncommon in real life (common on multiple choice tests). They are usually large at presentation
(larger than 3 cm). The look is variable (heterogenous, homogenous, cystic areas, calcifications,
sometimes even fat). Having said that, the most classic look is a heterogeneous mass with AVID
ENHANCEMENT. On MRI they are T2 bright. Both MIBG and Octreotide could be used (but
MIBG is better since Octreotide also uptakes in the kidney).

Gamesmanship: The hyper


enhancement washout trick. They
could show you what looks like an
adenoma study (multiple phases to
calculate washout) - but with
mega enhancement (HU > 120).
Remember, I don't care what the
fuck washout out numbers you get
- if they show you HU
measurements > 120 on arterial or
portal venous phase you can NOT
call the thing an adenoma.

Gamesmanship: This thing isn’t


always in the adrenals. They can Pheo at the Organ of Zuckerkandl - T2 Bright
be extra adrenal (organ of
Zuckerkandl - usually at the IMA).

“Rule of 10s”

10% are extra adrenal (organ of Zuckerkandl - usually at the IMA), 10% are bilateral, 10%
are in children, 10% are hereditary, 10% are NOT active (no HTN).

“Syndromes” MEN 2 (subtypes 2a and 2b)

Both subtypes of MEN 2 are associated with


Associated syndromes: First think Von Hippel
Pheochromocytomas (50% of patients).
Lindau, then think MEN IIa and IIb. Other
In the case of MEN 2 they usually occur
things less likely to be tested include NF-1, multiple and bilateral.
Sturge Weber, and TS.
MEN 2 + Adrenal Mass = Pheo

•“Carney Triad”

•Extra-Adrenal Pheo, GIST, and Pulmonary Chondroma (hamartoma).


•Don't confuse this with the Carney Complex
(Cardiac Myxoma, and Skin Pigmentation).

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ADH_2020
Other Misc Adrenal Masses:
Myelolipoma

Benign tumor that contains bulk fat. About 1/4 have


calcifications. If they are big (> 4 cm) they can bleed, and present
with a retroperitoneal hemorrhage. Another piece of trivia is the
association with endocrine disorders (Cushings, Congenital
Adrenal Hyperplasia, Conns).

Don’t get it twisted, these tumors are NOT functional, they just
happen to have associated disorders about 5-10% of the time.

Cyst - You can get cysts in your adrenal. They are often
unilateral, and can be any size. The really big ones can bleed.
They have a thin wall, and do NOT enhance.

Mets: Think breast, lung, and melanoma. They have no


specific imaging findings and look like lipid poor adenomas. Myelolipoma - Bulk Fat
If the dude has a known primary (especially lung, breast, or Hyperechoic on US
melanoma), and it’s not an adenoma then it’s probably a met.

Cortical Carcinoma:

These are large (4 cm -10 cm), may be functional (Cushings),


and calcify in about 20% of cases.

They arc bad news and often met everywhere (direct invasion
often first).

As a pearl, an adrenal carcinoma is not likely to be less than 5


cm and often has central necrosis.

Adrenal Cortical Carcinoma


-Direct invasion of the liver
Calcifications

This is often the result of prior trauma or infection (TB). Certain tumors (cortical carcinoma,
neuroblastoma) can have calcifications. Melanoma mets are known to calcify.

Wolman Disease: - This is a total Aunt Minnie (and massive


zebra / unicorn). Bilateral enlarged calcified adrenals. It’s a fat
metabolism error thing that kills (“booka” - Ali G) before the first year of
life.

352

ADH_2020
SECTION 2:
Syndromes

MEN: “Multiple Endocrine Neoplasia”

There are three of these stupid things, and people who write multiple choice tests love to
ask questions about them.

* MEN 1: Parathyroid Hyperplasia (90%), Pituitary Adenoma, Pancreatic Tumor


(Gastrinoma most commonly)

* MEN 2: Medullary Thyroid Cancer (100%), Parathyroid hyperplasia,


Pheochromocytoma (33%)

* MEN 2b: Medullary Thyroid Cancer (80%), Pheochromocytoma (50%), Mucosal


Neuroma, Marfanoid Body Habitus

MEN Mnemonics
MEN I (3 Ps)
- Pituitary, Parathyroid, Pancreas

MEN IIa (1M, 2Ps)


Medullary Thyroid Ca,
Pheochromocytoma, Parathyroid

MEN IIb (2Ms, 1P)


- Medullary Thyroid Ca, Marfanoid Habitus /mucosal neuroma,
Pheochromocytoma

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Carcinoid Syndrome:

Flushing, diarrhea, pain, right heart failure from serotonin manufactured by the carcinoid
tumor. The syndrome does not occur until the lesion mets to the liver (normally the liver
metabolizes the serotonin). The typical primary location for the carcinoid tumor is the GI
tract (70%). The most common primary location is the distal ileum (older literature says
appendix). The actual syndrome only occurs in 10% of cases - and is actually very rare (in
real life - not on tests).

Carcinoid -Classic Mesenteric Involvement

Trivia: GI carcinoids are associated with other GI tumors (GI adenocarcinoma).

Trivia: Urine Test for Carcinoid = 5-HIAA (5-hydroxyindoleacetic acid)

Trivia: Nukes Test of Choice: 111In-Octreotide (Octreoscan)

Trivia: MIBG is also positive - but less than 25% of the time (like 15%). Gallium is positive,
but super non-specific.

Trivia: Systemic serotonin degrades the heart valves (right sided), and classically causes
tricuspid regurgitation

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Hereditary Syndromes

Pheochromocytoma
Endolymph Sac Tumor is (risk ~10%). Less
Hemangioblastoma
common (~10%). likely to be
is the most
associated with
common tumor
Bilateral clear cell RCC catecholamine
VHL (seen in the
(~risk ~70%) production.
retina,
cerebellum, spinal
Papillary Cystadeoma of the Pancreatic Cysts
cord)
epididymis (~55%) (~75%) and serous
cystadeomas

Multiple head and


PGL Syndrome
neck Pheochromocytoma risk is variable depending on the
(Paraganglioma &
paragangliomas subtype
Pheochromocytoma)
(risk ~70%)

Cortical Tubers, Subependymal Renal AMLs (risk


Nodules, ~80%)
Clinical Triad
(Facial
Tuberous Sclerosis Subependymal Giant Cell Cardiac
Angiofibroma,
(Bourneville Disease) Astrocytoma (SEGA) - found at Rhabdomyoma
Seizures, Retard
the caudothalamic groove
Brain)
adjacent to the foramen of Pulmonary Cysts
monro LAM

Parathyroid Gastrinoma is the


Pituitary Primary Hyperparathyroidism is most common
Pancreas the most common (risk - pancreas /
100%), related to adenomas duodenal tumor —
MEN 1
Less commonly jejunal ulcers and
carcinoids of the Prolactinoma is the most gastric fold
bronchus, and common pituitary tumor thickening (Zollinger
bowel Ellison)

• Pheochromocytoma (~50%)
Medullary Thyroid
MEN 2 A and often bilateral
Cancer
• Primary Hyperparathyroidism Thyroid cancers
occur at younger
ages and are
• Marfanoid Appearance
Medullary Thyroid multicentric
• Mucosal Neuromas
Cancer
MEN 2 B • Intestinal Ganglioneuromas
Elevated levels
• These patients fart alot
Pheochromocytoma of calcitonin cause
(seriously)
flushing and
Can be diarrhea similar to
Familial Medullary considered a carcinoid syndrome
Thyroid (FMTC) subtype of MEN 2

355

ADH_2020
SECTION 3:
Thyroid

Anatomy: The thyroid gland is a butterfly shaped gland, with two lobes connected by an
isthmus. The thyroid descends from the foramen cecum at the anterior midline base of the
tongue along the thyroglossal duct. The posterior nodular extension of the thyroid (Zuckerkandl
tubercle) helps give a location of the recurrent laryngeal nerve (which is medial to it).

Thyroid Nodules: Usually evaluated with ultrasound. Nodules are super super common and
almost never cancer. This doesn’t stop Radiologists from imaging them, and sticking needles
into them. Ultrasound guided FNA of colloid nodules is a major cash cow for many body
divisions, that on very rare occasions will actually find a cancer. Qualities that make them more
suspicious include: more solid (cystic more benign), calcifications (especially
microcalcifications). Microcalcifications are supposed to be the buzzword for papillary
thyroid cancer. “Comet Tail” artifact is seen in Colloid Nodules. “Cold Nodules” on I-123
scans are still usually benign but have cancer about 15% of the time, so they actually deserve
workup.

Colloid Nodules: These are super super common. Suspicious features include
microcalcifications, increased vascularity, solid size (larger than 1.5 cm), and being cold on a
nuclear uptake exam. As above, Comet tail artifact is the buzzword.

Ultrasound Characteristics of Thyroid Nodules

Margins & Size &


Calcifications Vascularity Echotexture
Shape Multiplicity

Increased Risk Complete Peripheral Solid composition has Nodule size is


• Micro x3 hypoechoic pattern of flow the highest sensitivity NOT predictive of
• Macro x2 halo is highly is suggestive of for malignancy malignancy.
suggestive of benign disease (although not specific
benign disease - many benign nodules Suspicious
Microcalcifications have Central pattern are also solid.) features should be
the highest accuracy, of flow is the primary
Pure cystic, or
specificity, and positive suggestive of consideration
spongiform with more
predictive value for malignancy when targeting for
than 50% specific are
detecting malignancy biopsy (not size)
likely benign.
Microcalcifications = the
“hallmark” of papillary CA

Macrocalcification - most Irregular, Solid Change over time Multiple nodules =


common calcification in spiculated, & hypervascular from solid to cystic decreased cancer
medullary CA microlobulated nodules are suggests benign rate per nodule —
margins more likely to disease but the overall
suggest be malignant rate of having
Macrocalcifications in a malignancy Most hyperechoic or cancer in one
single nodule = higher risk isoechoic nodules are nodule is fairly
benign. constant.
Macrocalcifications in a
multi-nodule goiter = lower Solid Hypoechoic =
risk feature of
malignancy

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Thyroid Adenoma: These look just like solid colloid nodules on ultrasound. They can
be hyper functioning (hot on uptake scan). Usually if you have a hyper-functioning nodule
(toxic adenoma), your background thyroid will be colder than normal (which makes sense).

Goiter - Thyroid that is too big. In North America it’s gonna be a multi-nodular goiter or
Graves. In Africa it’s low iodine. You can get compressive symptoms if it mashes the
esophagus or trachea. These are often asymmetric - with one lobe bigger than the other.

Subacute Thyroiditis / De Quervains Thyroiditis: The classic clinical


scenario is a female with a painful gland after an upper respiratory infection. There is a
similar subtype that happens in pregnant women, although this is typically painless. You get
hyperthyroidism (from spilling the hormone) and then later hypothyroidism. As you get over
your cold, the gland recovers to normal function. Radiotracer uptake will be decreased during
the acute phase.

Acute Suppurative Thyroiditis: This is an actual bacterial infection of the thyroid.


It is possible to develop a thyroid abscess in this situation. A unique scenario (highly
testable) is that in kids this infection may start in a 4th branchial cleft anomaly (usually
on the left), travel via a pyriform fistula and then infect the thyroid. Honestly, that is
probably too much for the exam - but could show up on a certification exam under neuro.

Reidels Thyroiditis: This is one of those IgG4 associated diseases (others include
orbital pseudotumor, retroperitoneal fibrosis, sclerosing cholangitis). You see it in women in
their 40s-70s. The thyroid is replaced by fibrous tissue and diffusely enlarges causing
compression of adjacent structures (dysphagia, stridor, vocal cord palsy). On US there will
be decreased vascularity. On an uptake scan you are going to have decreased values. A
sneak trick would be to show you a MR (it’s gonna be dark on all sequences - like a fibroma).

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Thyroglossal Duct Cyst (TGDC): The
most common congenital neck cyst in Pediatrics.
This can occur anywhere between the foramen
cecum (the base of the tongue) and the thyroid
gland (or below). It looks like a thin walled cyst.

Why Care?
• They can get infected
• They can have ectopic thyroid tissue
• Rarely, that ectopic tissue can get Thyroglossal Duct Cyst - Midline

papillary thyroid cancer (if you see an


enhancing nodule)

TGDC - Location Fuckery


These are the general numbers to think about:
Suprahyoid = 25%
At the Hyoid = 30%
Infrahyoid = 45%

So, where is the most common location?


Well, it depends on how they ask. If all things are equal the answer is Infrahyoid (which seems
counterintuitive based on the embryology but is non the less true).
BUT - if "at or above the hyoid” is a choice - then that is actually the right answer
(25+30 > 45). As always, read every choice carefully.

Ectopic and Lingual Thyroid: Similar to a thyroglossal duct cyst, this can be found
anywhere from the base of the tongue through the central neck. The most common location
(90%) is the tongue base (“Lingual Thyroid”). It will look hyperdense because of its
iodine content (just like a normally located thyroid gland). If you find this, make sure you
check for a normal thyroid (sometimes this is the only thyroid the dude has). As a point of
trivia, the rate of malignant transformation is rare (3%).

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Graves - Autoimmune disease that causes hyperthyroidism (most common cause). It’s
primarily from an antibody directed at the TSH receptor. The actual TSH level will be low.
The gland will be enlarged and “inferno hot” on Doppler.

• Graves Orbitopathy. Spares the tendon insertions, doesn’t hurt (unlike pseudotumor).
Also has increased intra-orbital fat.

• Nuclear Medicine: Increased uptake of I-123 %RAIU usually 50-80%. Visualization of


pyramidal lobe is accentuated.

Hashimotos - The most common cause of goitrous hypothyroidism (in the US). It is
an autoimmune disease that causes hyper then hypothyroidism (as the gland burns out later).
It’s usually hypo - when it’s seen. It has an increased risk of primary thyroid lymphoma.
Step 1 trivia; associated with autoantibodies to thyroid peroxidase (TPO) and anti­ thyroglobulin.

On Ultrasound:
There are two classic findings;

(a) Heterogeneous “giraffe skin” appearance,

(b) White Knights - uniform hyperechoic nodules -


which are actually regenerative nodules.

Level 6 Nodes - “Delphian Nodes”


- These arc the nodes around the thyroid in the front of the neck.
- You can commonly see them enlarged with Hashimotos.
- However, for the purpose of multiple choice tests, a sick looking level 6 node - or
“Delphian Node” is a laryngeal cancer met.

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Thyroid Cancer: You can get lots of cancers in your thyroid. There are 4 main subtypes
of primary thyroid cancer. Additionally you can get mets to the thyroid or lymphoma in your
thyroid - this is super rare and I’m not going to talk about it.

Microcalcifications is Mets via the


The Most Common the buzzword and lymphatics. Has an
Papillary Subtype. “Papillary is key finding (seen in overall excellent
Popular” the cancer and prognosis, and
nodes). responds well to I-131.

Mets hematogenously
to bones, lung, liver,
The second most etc.. Survival is still
Follicular common subtype. ok, (less good than
papillary). Does
respond to I-131.

Tendency towards
Association with local invasion, lymph
MEN II syndrome. nodes, and
Medullary Uncommon
Calcitonin production hematogenous spread.
is a buzzword. Does NOT respond to
I-131.

Seen in Elderly. Seen Rapid growth, with


in people who have primary lymphatic
Anaplastic Uncommon
had radiation spread. Does NOT
treatment. respond to I-131.

Does not take up


I-131 as well as
Hurthle Cell (variant Seen more in Elderly. normal follicular.
Uncommon
of Follicular) FDG-PET is the way
to go for surveillance.

Metastasis: The buzzword is going to be microcalcifications in a node (with papillary).


The nodes are typically hyperechoic compared to regular nodes, hyperenhancing on CT, and
T1 bright on MR. Remember that thyroid cancer is hypervascular, and it can bleed like stink
when it mets to the brain. If there are mets to the lungs, the classic pattern is “miliary.” The
additional pearl with regard to lung mets is that they can be occult on cross sectional imaging,
and only seen on whole body scintigraphy. For the purpose of multiple choice tests pulmonary
fibrosis is a risk of treating with I-131 if you have diffuse lung mets.

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ADH_2020
SECTION 4:
Para-Thyroid

Anatomy: There are normally 4 parathyroid glands located posterior to the thyroid. The
step 1 trivia is that the superior 2 are from the 4th branchial pouch, and the inferior 2 are
from the 3rd branchial pouch. The inferior two are more likely to be in an ectopic location.

Parathyroid Adenoma: This is by far the most common cause of


hyperparathyroidism (90%). On ultrasound these things look like hypoechoic beans
posterior to the thyroid. A 4D-CT can be used to demonstrate early wash-in and delayed
wash-out. Nuclear medicine can use two techniques (1) the single-tracer, dual-phase
Sestamibi, or (2) the dual tracer Sestamibi +I-123 (or Pertechnetate). These arc discussed
in detail in the nukes section.

Parathyroid Adenoma - 4D CT shows early enhancement, and delayed washout

Parathyroid Carcinoma: This is pretty uncommon, and only makes up about 1% of


the causes of hyperparathyroidism. It looks exactly like an adenoma on imaging. The only
way you can tell on imaging is if they show you cervical adenopathy or invasion of adjacent
structures.

High Yield Parathyroid Trivia:


Q: What are the causes of hyperparathyroidism?
A: Hyperfunctioning Adenoma (85-90%),
Multi-Gland Hyperplasia (8-10%), Cancer (1-3%).
Q: What factors does sestamibi parathyroid imaging depend on?
A: Mitochondrial density and blood flow

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