2. Pathology II Flashcards by J L

Hyperadrenocorticism (Cushing syndrome)
• Chronic exposure to high levels \_\_\_\_
• ACTH-dependent or ACTH-independent
• Most cases \_\_\_\_
• Other etiologies
– \_\_\_\_ tumor (Cushing disease)
– \_\_\_\_-secreting tumors
– \_\_\_\_ disease

• Cushing disease causes syndrome, and causes pigmentation; cushing syndrome doesn't always cause \_\_\_\_
• Can get cushing's without altering adrenal gland > giving patient chronic prednisone
	○ Iatrogenic is the most common cause
• Can get ACTH-dependent or independent
	○ Dependent
		§ \_\_\_\_ gland produces ACTH > adrenals at high levels > high steroid
	○ Independent
		§ Not pit causing the problem, but something within the \_\_\_\_ gland > a tumor (functional) in the cortex
		§ Iatrogenic

• Face becomes big and round
	○ Become more \_\_\_\_
• Gaining weight
• \_\_\_\_

glucocorticoids
iatrogenic
pituitary
steroid
genetic

pigmentation
pit
adrenal

edematous
osteoporosis

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Clinical manifestations

____ gain
Easy bruising
Moon ____
Abdominal striae
____ weakness
Fatigue
____
Acne and other infections
____ disorders
Hypertension
____
Irregular menstruation
____
Back pain
____ hump
Erectile dysfunction
Mucocutaneous ____

weight
facies
muscle
osteoporosis

mood
diabetes
hirsutism
buffalo
pigmentation

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• Pigmentation a conseq of cushing ____ not ____
○ Syndrome may be ACTH-indepdnent
§ Pigmentation only occurs in presence of ____ overexpression (and ACTH therefore)

DISEASE
SYNDROME
MSH

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Treat underlying cause
Reduce corticosteroid intake
Block cortisol synthesis
____ (Nizoral®)
Mitotane (Lysodren®)
____ (Metapirone®)
Control cortisol tissue effects
____ (Korlym®)
Bilateral adrenalectomy
Inoperable pituitary tumor
Refractory cases• Cushing disease
○ Treat the brain
○ Remove the pathology of the pit
• Cushing syndrome
○ Treat the cause
§ Too much steroids - stop the medication, carefully!
□ If giving patient prednisone for a few weeks > the patients adrenals will shut down entirely > body senses steroids in the system and systemically, the adrenals shut down, when taken off > take them off ____ > need adrenals to readapt decreased steroids in the circulation
® These patients still retain FFF response - and in a stressful situation in a dental office > if taking prednisone and you stop it > may experience an adrenal crisis > body is trying to respond to FFF, but it can’t do it > body crashes
® Pills from 40, 20, 10, 5mg > tapers you down to make sure you don’t experience an adrenal crisis
○ Reduce steroid production from adrenals, or reduce effect of steroids on the downstream tissues > ____ > prevents cortisol (steroid) synthesis from the adrenal gland
§ Used for ____ infections
□ Including patients w ____ disease
® High risk of developing adrenal insufficiency bc of the drugs they’re taking (in addition to protease inhibitors)
○ Drugs that control cortisol on downstream tissues
§ Mifepristone
○ Surgical excision if medication fails > supplement w steroids to maintain normal levels

ketoconazole
metyrapone

mifeprestone

slowly
ketoconazole
fungal
HIV

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Adrenocortical insufficiency (Addison disease)

• Primary
– Destruction or dysfunction of ____
– Only form that induces ____

• Secondary
– Reduced pituitary ____ secretion

• Tertiary
– Reduced ____ secretion

• Important cause of mucocutaneous pigmentation, but not all causes of addisons trigger pigmentation
	○ Only addisons caused by \_\_\_\_ pathology to the adrenals cause pigmentation
		§ That's what triggers ACTH to be released from the brain
• Can get secondary addisons, or tertiary addisons
	○ Secondary addisons > reduced pituitary ACTH secretion
		§ Hypopit > decreased ACTH > not enough steroids produced, and the adrenals are hypo-active
		§ Won't cause \_\_\_\_, bc ACTH is reduced
	○ Tertiary
		§ If hypo reduces CRH secretion > less ACTH > less activity from the glands
		§ No \_\_\_\_

adrenal cortex
pigmentation

ACTH

hypothalamus CRH

primary
pigmentation
pigmentation

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Primary adrenocortical insufficiency

• Most often due to autoimmune destruction
– ____
– Anti-21-hydroxylase enzyme

• Infection
– ____
– Fungal
– ____

anti-adrenal antibodies
mycobacterial
AIDS

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Primary adrenocortical insufficiency
• Cancer

• Bilateral adrenal hemorrhage
– Adults – ____
– Children – ____

• Taking warfarin or cumidine > excessive bleeding from the glands
	○ In adults
• In children > WFS

anticoagulant therapy

waterhouse-friderichsen syndrome

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Adrenocortical insufficiency
ACTH accumulates within blood (____ disease only) Systemic complications
Diffuse mucocutaneous ____
Treat by ____ therapy

primary
pigmentation
replacement

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Cushing disease vs Addison disease

Dexamethasone suppression test
Measures suppression of ACTH secretion from pituitary
1. Measure ____ level in morning
2. 1 mg of ____ at 11 p.m.
3. Measure cortisol following morning
If ACTH not suppressed, then cortisol levels remain ____

ACTH stimulation test
1. Measure cortisol level in morning 
2. \_\_\_\_ injection
3. Blood drawn after 60 minutes
4. Measure cortisol
Increase in cortisol after stimulation by ACTH then adrenals are \_\_\_\_

• Addison's can be dx via ACTH stim test
	○ Makes use of synthetic analog of ACTH
	○ First in morning > blood drawn > measure baseline cortisol
	○ After blood draw > injected IV w ACTH analog (cosyntropin) > one hour later > blood drawn again > cortisol measured a second time
		§ If adrenals are proper fxn > analog stim should inc cortisol
		§ If doesn't stim cortisol after an hour > glands not fucntioning properly > dx addison's
• Cushing disease is tested w the dexamethasone suppression
	○ Patient in morning gets blood drawn and cortisol measured
	○ Befroe bed > take oral dosage of steroid (dexamethasone)
	○ Next morning in lab > blood draw > measure steroid levels
		§ Normal circumstances > big dose of steroid > suppress ACTH and suppress further steroid release from the adrenals
		§ If doesn’t > ACTH const expressed from the pit > indicative of cushing's disease
• Usually dex first, ACTH stim second

cortisol
dexamethasone
high

cosyntropin
normal

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Hyperaldosteronism

• Primary (Conn syndrome)
– Usually due to functional ____

• Secondary
– Due to excessive ____ secretion

• Conn
	○ Tumor in adrenal that's producing aldosterone
		§ Goes to kidney > complications that arise from aldosterone activity
			□ Patient will have \_\_\_\_, \_\_\_\_ and \_\_\_\_ (alkalosis)

• Secondary
	○ Adrenals function properly, except the \_\_\_\_ is not fucntioning properly in the kidney
	○ Kidmey insenstive to aldosterone > renin secretion from the kidney > goes to adrenal gland to produce ald > does what it does on the kidney
	○ Same result

adenoma
renin

HTN
hypokalemia
alkalotic

aldosterone

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Thyroid gland
• \_\_\_\_ neck
• Originates from base of \_\_\_\_
• Composed of thyroid follicles
– Contain \_\_\_\_
• Hormones and Iodine

• On the backside of the thyroid are the parathyroids
• Physically attached at the level of foramen cecum, and then the stalk of tissue is dissolved throughout development
	○ IF not > \_\_\_\_ duct cyst
• Follicles are lined by \_\_\_\_ epi cells
	○ The pink stuff is \_\_\_\_ material
		§ Fluid
		§ Composed of hormones and iodine
			□ Hormone = \_\_\_\_ (makes up the colloid)
• Bt the follicles > parafollicular cells
	○ \_\_\_\_
		§ Directly and completely counteracts action of PTH
			□ Work on bone and kidney (same structures)
• T3 and T4
	○ Produced from thyroglobulin
	○ \_\_\_\_ cells (cuboidal) upon stim > convert thyroglobulin to T3 and T4
		§ Once produced > enter circulation

anterior
tongue
colloid

thyroglossal
cuboidal
colloid

thyroglobulin
calcitonin

follicular

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Thyroid gland
• Follicular cells produce
– \_\_\_\_
– \_\_\_\_
– \_\_\_\_

• Parafollicular cells produce calcitonin
– Regulates ____ metabolism
– Antagonist to ____

thyroglobulin
triiodothyronine (T3)
thyroxine (T4)

calcium
parathyroid hormone

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Hypothalamus-pituitary-thyroid axis

Hypothalamus > ____

Pituitary > \_\_\_\_
Thyroid 
> TSH binds to TSH-receptor (TSH-R) 
> Converts thyroglobulin to \_\_\_\_
- T3 / T4 bound to \_\_\_\_, transthyretin, thyroxine-binding globulin

• Three organs work synergistically, part of the same axis
	○ Begins with hypo > produces TRH > acts on the pit to stim TSH > acts on thyroid follicles to trigger conversion thyroglobulin to T3 and T4
	○ TSH binds to TSH receptor on follicular cells > once binds > cascade of events
		§ Most hormones act through G protein receptor > cascade that's mediated via \_\_\_\_ (and \_\_\_\_) (propagates signal into cell)

TRH
TSH
T3 and T4
albumin

cAMP
adenylate cyclase

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• Organs affected by T3/T4
		○ \_\_\_\_ development
		○ Brain
		○ \_\_\_\_
		○ Skin
		○ \_\_\_\_ rate

eye
kidney
heart

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Thyroid diseases
• Hyperthyroidism 
• Hypothyroidism 
• Developmental
• Goiter
  • Neoplasia

	• When hormone levels are out of whack > things go awry
	• Goiter
		○ Enlarged \_\_\_\_ gland
		○ \_\_\_\_ of the thyroid manifesting as a diffuse mass of the thyroid
	• Hypothyroidism
		○ Slowing of \_\_\_\_
	• Hyperthyroidism
		○ Accel of \_\_\_\_
		○ Nervous, agitated

thyroid
hyperplasia
metabolism
metabolism

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Hyperthyroidism
• Graves disease due to \_\_\_\_ autoantibodies
• Pituitary tumor secreting \_\_\_\_
• Excessive TRH from \_\_\_\_
 • Serum thyroid hormones elevated
• Plasma TSH elevated or suppressed

• Hyperactivity = hyperthyroidism
	○ Most common development > graves disease
		§ \_\_\_\_ disease
			□ \_\_\_\_ mechanism
			□ Autoab to TSH receptor on follicular cells > once ab binds to the receptor > overactivates > const activated > whole cascade happens ove r and over again
				® Thyroglobulin cont converted to T3 and T4
	○ Tumor
		§ Producing TSH > cont stimulating receptor and producing T3 and T4
	○ Pathology of hypothalamus
		§ Excessive secretion of TRH > pit > high levels of TSH
• Treatment pit patholgy diff from graves disease, etc.
	○ For a pit tumor > treat w surgery
	○ For graves dx > require \_\_\_\_ therapy, or surgery of the thyroid
• T3 and T4 are elevated, TSH may be elevated or not
	○ Bc of negative feedback mechanism
	○ Specifically in context of Grave's dx

TSH-R
TSH
hypothalamus

autoimmune
type II
medicinal

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Graves disease

• Most common cause of hyperthyroidism 
– \_\_\_\_ with genetic component
• \_\_\_\_>>M
• \_\_\_\_ thyroid enlargement
• Autoantibodies to TSH-R
– Thyroid stimulating immunoglobulin
– TSH levels \_\_\_\_
• untreated hyperthyroidism may lead to \_\_\_\_

multifactorial
F
symmetric
reduced
thyroid storm

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Graves disease

• Commonly manifesting in older females
• Have a \_\_\_\_ (thyroid enlargement)
• Mechanistically
	○ Developing autoab to the TSH receptor > binding receptor > triggering activation of receptor constantly > conversion of thyroglobulin to T3 and T4
	○ TSH reduced
		§ Activated > brain thinks TSH isn't needed anymore > hypo is sensing, and asking why producing more?
			□ Result is that the brain shuts down TSH secretion and production > bc the \_\_\_\_ mistakenly thinks it has enough already
• [???]
• Patients w hyperthyroidism > \_\_\_\_ metabolism, eat a lot (not bc overly hungry but bc they're using all the energy theyr'e getting), inc appetite, palpating very quickly, jittery 
• Thyroid storm
	○ Life threatning complication > in response to underlying \_\_\_\_ state that releases TSH under normal circumstances > may result in more activation of the thyroid beyond what they're currently experiencing
		§ More exacerbated phenotypes
		§ May die of a \_\_\_\_
• Follicles are mishapen, the colloid is less pink (not uniform)
	○ Spcaes bt the colloid and the actual cells
	○ \_\_\_\_ has been converted to T3 and T4 (less of it in the follicle)

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goiter
brain
rapid
stressful
heart attack
colloid

Clinical manifestations

• Array of complications for Graves
	○ Excessive \_\_\_\_
	○ Hair loss and thinner hair
	○ \_\_\_\_ start flaking off
	○ Moist skin
	○ \_\_\_\_ damage (cannot keep up w metabolic demand)
	○ Weakness of bone (osteoclasts are helping to resorb bone - bone's not keeping up w the demand)
	○ \_\_\_\_ (irregular beat, rapid pulse)
	○ Protrusion of eyeballs (not patho)
	○ \_\_\_\_ loss (even though eating a lot, losing a lot of weight)

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hunger
nails
muscle
heart
weight

Hypothyroidism

____
Hashimoto thyroiditis
Congenital (____)
Severe iodine deficiency• Exact opposite in terms of manifestations
○ Not as hungry
○ Hair is not healthy looking
○ Skin is dry
○ ____ are unaffected
○ Weight gain
○ HR slows down, bc the metabolism has decreased
• Most common cause - ____
○ Autoimmune
• Severe hypothyroidism > ____ (also used to describe congential hypothyroidism)
• Table salt is supplemented w iodine > prveents hypothyroidism
• Thyroid can be dysfunctional bc of:
○ At the level of thyroid
○ Hypopit can cause hypothyroidism
○ Hypothalamus shuts down > CRH drops > thyroid hormone levels drop
○ Like w diabetes, or adrenals > downstream organs insensitive of T3/T4 > hypothyroidism
§ Born/develop mutation in T3 T4 receptor > defect found in cell that require hormone > tissues are less sensitive to the hormone

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surgery
myxedema
eyeballs
hashimoto thyroiditis
myxedema

Hypothyroidism

• Skin tone is \_\_\_\_
• Mental state and self esteem goes down
	○ Strong \_\_\_\_ component

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duller

psychological

Hashimoto thyroiditis

• Most common cause of \_\_\_\_
• \_\_\_\_ destruction of thyroid follicles with lymphocytic infiltrates
– May occur after \_\_\_\_
• Gland \_\_\_\_
• Treat with \_\_\_\_

• Autoimmune, unlike graves > the follicles look normal, what's not normal > lymphoid aggregates within the glandular tissue
	○ Blue things on the slide
		§ \_\_\_\_
		§ Helps destroy the glandular tissue
• Formation of autoab's that aggravate the state
• Over time > the gland shrinks
• Not producing TRH, or TSH from the pit > if your thyroid is not responsive to TSH or CRH > then the gland will also shrink
• Treatment is not easy, may require surgery or medications that will reduce the formation of antibodies in GRAVE's
	○ In hypothyroidism > prescribe levothyroxine (synthyroid) > replaces \_\_\_\_

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hypothyroidism
autoimmune
hyperthyroidism
shrinks
levothyroxine

t cells and b cells
T3 and T4

Hashimoto thyroiditis
• Autoantibodies 
– \_\_\_\_
– \_\_\_\_ blocking
– \_\_\_\_

TSH elevated
____ increases susceptibility• Abs to thyroglobulin
○ Destory and prveneting conversion to T3 and T4
• Can block activation of receptor > TSH-R blocking
• May have ab to thyroidal peroxidase > conevrsion of thyroglobuin to T3 and T4
• TSH is elevated > bc not producing T3 and T4 > result is that the pit senses that more TSH should be secreted > pit producing more TSH in repsonse
• Not a ____ disease, but a link > runs in families (not 1:1) > inc risk of developing hashimoto

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thyroglobulin
TSH-R
thyroidal peroxidase

HLA-DR5

genetic

Clinical manifestations

• Hypothyroidism
	○ Skin, hair and eyes changed before and after
• Patients have \_\_\_\_ metabolism > to the point that if you offer them certain drugs > drugs may not \_\_\_\_ properly
	○ One particular instance > prescribing opioids to these patients > opioids reduce metabolism on their own to their background condition > double-whammy > could lead to \_\_\_\_ or death
		§ Not ever prescribed an opioid!

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slower
metabolized
coma

``` Congenital hypothyroidism (Myxedema, Cretinism) • 1 in 4000 births • ____:M, 2:1 • ____ / hypoplasia of thyroid • Defective ____ biosynthesis • Mental ____ ``` • Severe hypothyroidism > myxedema or congenital hypothyroidism > born being hypothryoid > developmental of the thyroid gland where patients don't have enough thyroid being formed • More commonly seen in girls (not boys) • If thyroid developent is perturbed > hypoplasia or aplasia > most important reasons for being hypothyroid at birth • Gland may be ____, but mutation in gene or protein > inhibits proper hormone biosynthesis • Earlier the onset > more likely the kids will be born severly ____ delated • Severe adult case > myxedema > severe hypothyroidism ○ After treatment > feet and face returned to ____ • Coma is a possibility ○ Add opioid on top of hypothyroid > develop death

F aplasia hormone retardation normal developmentally normal

``` Lingual thyroid • Developmental failure of thyroid to descend • ____ >> M • Most patients are ____ • Treat with ____ ``` • Thyroid develpos from ____ > migration never happens in some patients > develop w a thyroid in the post region of mouth in base of tongue area > they never descended • Bc of where they are anatomically > invariably these patients will become ____ > treated w levothyroxine • Rare cases > compeltely ____ > euthyroid > normal > never will be hypothyroid unless develops another dx that exarcesbates • Don’t treat > functional thyroid tissue, but not enough functional thyroid ○ Does not warrant a ____ ○ The mass is very vascular, and bc of anatomical location > indicative of what it is clinically

F hypothyroid levothyroxine foramen cecum hypothyroid normal biopsy

Goiter • Diffuse thyroid enlargement due to prolonged stimulation by ____ ``` • Multiple causes – ____ deficiency or excess – Hashimoto thyroiditis – ____ disease – Pituitary adenoma – Dietary ____ – Goitrogenic medications ``` • Can be in hyperthyroidism or hypothyroidism • Hyperplasia of the thyroid gland via stim via TSH ○ Hyperactivity and enlarged gland compensating for the hyperactivity • This is why table salt is iodinated • Grapefruit can result in goiter

TSH iodine graves goitrogens

Thyroid neoplasia • Follicular adenoma – Most ____ tumor • Papillary carcinoma – Most common ____ – Usually history of ____ exposure • Medullary carcinoma – Cancer of ____ cells – Produces ____

``` common malignancy radiation parafollicular C amyloid ```

Thyroid neoplasia • Follicular adenoma ○ Follicle cells are neoplastic > mass in thyroid ○ Look at the neck of patient and the enlargement is ____ > NOT A TUMOR, mor likely to be a goiter § If asymmetric > most likely to be a ____ in the gland and not goiter ○ Most common cause of unilateral enlargement > ____ > may be FUNCTIONAL (can develop hyperthyroidism) • Most common cancer of thyroid > papillary carcinoma ○ Radiation exposure is a common factor ○ After meltdown in ____ > epidemiologic study > following kids over time to assess risk of papillary carcninoma as a result of the H bombs ○ Radiologists have a higher chance of developing as well • Medullary carcinoma ○ Produce calcitionin > bones bc denser § Preserves ____ in the bone ○ Produce amyloid § Commonly found in multiple myeloma § Looks ____ under the microscope > quite aggressive > affiliated w a genetic disease • ____ is the primary mode of treatment ○ If benign > excise the portion of the gland w the tumor ○ ____ next, and chemo if necessary

symmetric tumor follicular adenoma Japan calcium pink surgery radiation

Parathyroid gland ____ on each side Located on ____ ____ cells synthesize parathyroid hormone – Regulates calcium and phosphate in blood * There's four total * Regulates calcium by acting on the bone (any bone), or acts on kidney to stim vit D synthesis > goes to gut and reabsorbed CaPO43- from food > inc Ca2+ in circ

two posterior thyroid chief

• Type 1 and Type 2 PTH receptors – ____predominant • PTH and calcitonin oppose each other ``` • Two types of PT receptors ○ Type 1 § Found in all ____ § Kidney § More common ○ Type 2 § Some ____ and kidney • PTH ____ ca2+ release, calcitoini ____ Ca2+ release ○ Counteract each other ```

bones bones stim inhib

* Released when the body senses a low Ca2+ state > hypocalcemia > ____ is released > acts on kidney and bones to increase Ca2+ mobilization from the bone, and acts on vitamin D > activated > helps reabsorb Ca2+ from food products > all to help promote Ca2+ localization into the BS to restore Ca2+ levels * Ca2+ levels higher > ____ is secreted

PTH | calcitonin

Primary hyperparathyroidism • Excessive PTH from parathyroids • Caused by – Parathyroid ____ – Parathyroid ____ – Parathyroid hyperplasia of ≥ ____ glands • Secondarily > patients have kidney failure > secondary hyperPTH • Primary hyperPTH > primiarly presents from PT gland > xs productino of PTH bc of tumor, cancer or hyperplasia of >2 glands ○ More PTH being released > more Ca2+ being immobilized from the bones and intestine • Normal ca > ____ mg/dL > higher is hyperPTH ○ 12-13+ > hypercalcemic, and having hyperPTH

adenoma carcinoma 2 10

Secondary hyperparathyroidism Chronic ____ failure Severe ____ ____ deficiency • When dx is manifesting from a kidney dx > chronic renal failure ○ Kidney dysfunctions > asborption of fluids and Ca PO43- metbaolism/reabsorption ○ Vitamin D is not being produced properly > not acting on intestines to reabsorb Ca from food > hypocalcemic state > PT produces more PTH

renal hypocalcemia vitamin D

Clinical manifestations • Primary mechanism of getting Ca is through bone ○ ____ (weak bones) or ____ (weak and structurally deficient bone - highly prone to fracture) • PTH has other effects elsewhere in the body ○ ____ problems ○ Dizziness/nervous ○ ____ ○ Bone problems/joint problems

osteopenia osteoporosis digestive irritability

Clinical manifestations • Don't memorize the criteria for diagnoising osteopenia/porosis • Diagnosed via a bone scan > DEXA boen scan > inject radioactive dye > scan patient and wherever the dye lights up = bone is not strong in those areas ○ The higher the score > better ____ ○ Lower score > lower ____ > more likely to be ____

density densisty osteoporosis

• Brown tumors ○ Not tumors > ____ found in any bone in a multifocal pattern > highly characteristic of ____ (primary or secondary) § Especially in an ____ patient • Microscopically > central giant cell granulomas

CGCG hyperPTH older

Subperiosteal resorption • Prone to other bone defects esp in the periphery > ____ bones may become narrow > subperiosteal resorption ○ Treat primary path first > give patients ____, encourage taking calcium pills • If chronic renal failure > ____; and will restore some of the calcium

finger bisphosphonates dialysis

Hypercalcemia of malignancy ``` • Solid tumors may produce PTH-related protein – Acts on ____ receptor • Solid tumor metastases • ____ • PTH levels remain unchanged ``` • Upon metastasis > extension mobil of ca from the bones ○ Cancers may produce PTH-related protein > molecular mimic to PTH > can act on PTH 1 receptors (prim on the bones) ○ When cancers metastasize > produce ____ protein > stimulating the receptor on bones to help stimulate calcium mobilization > patients who have hypercalcemia malginancy > patients who have broadly ____ dx, or dx that affects bones (____) > sig calcium mobil from the bones > hypercalcemic § The ____ levels are unchanged § Not a consequence of PTH > they may ____, bc the body senses it doesn't need PTH • Treat w ____ to prevent bone resorption ○ IV bisphophonates § Risk > MRONJ

type I PTH multiple myeloma mimicry metastatic MM PTH

Multiple endocrine neoplasia • Autosomal ____ • MEN Type 1 – Mutation in tumor suppressor ____ • MEN Type 2 (aka 2A) and 3 (aka 2B) – Mutation in ____ ``` • Type 1 ○ Mutation in MEN1 • Type 2 and 3 ○ Mutation in RET ○ Similar except 3 has relevance to dentists > characterized by development of ____ of oral soft tissues and other soft tissue sites ○ Pheochromocytomas ○ Thyroid carcinomas ○ Parathyroid hyperplasia ○ Tall, gangly (look like Marfan) • Know the chart ```

MEN1 | proto-oncogene RET

``` • MEN 1 ○ Diamond § ____ § ____ § ____ lesions • MEN 2A/2B ○ ____ ○ ____ ```

pit parathyroid panc parathyroid pheo

Mucosal neuromas • Lips, tongue, ____ • Neuromas of ____, GI tract, bronchi • ____ histology

commissures eyes pathognomonic

McCune – Albright syndrome ``` • ____ somatic mutation • ____ spots • Precocious ____ • Multiple endocrinopathies – ____ – Adenomas of endocrine organs – ____ syndrome – Acromegaly – Benign ____ cysts ``` • Not a genetic disease > sporadically occurring disease ○ Occurs after fertilization ○ ____ disease • Café-au-lait spots • Polyostotic fibrous dysplasia ○ Common disease in the jaw bones • Prone to several endocrinopathies ○ Gene regulates endocrine function § Prone to pit adenomas, ovarian pathology, precocious puberty, agromegaly □ Depending on when exposed > predisposes to various

``` GNAS1 cafe-au-lait puberty hyperthyroidism cushing ovarian ``` somatic

Hyperparathyroidism – jaw tumor syndrome * Germline mutation in ____ tumor suppressor * ____ or carcinomas * ____ * Polycystic ____ disease • When HRPT2 mutated in germline > hyperPTH jaw tumor syndrome ○ Patients develop parathyroid (adenomas or carcinomas; primary) and jaw tumors (ossifying fibromas) and kidney disease

HRPT2 parathyroid adenomas ossifying fibromas kidney

2. Pathology II Flashcards

(44 cards)