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MSY2 Repro/Endo > Rapid Review > Flashcards

Rapid Review Flashcards

1
Q

In what type of neoplasm are schiller-Duvall Bodies seen?

What is their characteristic histological appearance?

A

Seen in endodermal sinus tumor / Yolk Sac Tumor (germ cell tumors) of the ovaries.

Have a “gomerulus-like” appearance/structure

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2
Q

In what tumor would you see call-exner bodies

what is their histological appearance?

A

Call-exner bodies are seen in granulosa cell tumors of the ovaries.

They are gland like structuers with esoinophilic material

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3
Q

Where do you see Reinke Crystals?

A

Sertoli-Leydig cells tumors of the ovary

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4
Q

What is Meigs Sydrome?

With what pathology woud you classically see Meigs Syndrome?

A

Meigs Syndrome consists of the triad:

Right side pleural effusion, asciteis, ovarian mass

Seen in Thecoma-Fibroma neoplasms of the ovary

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5
Q

What is a tumor marker for dysgerminoma?

A

LDH serum

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6
Q

What would be a tumor parker for endodermal sinus tumor / yolk sac tumor?

A

AFP

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7
Q

What type of histology do choriocarcinoma consist of?

A

placental tissue with trophoblasts and syncyciotrophoblast with NO VILLI

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8
Q

synthetic estrogen DES is associated with what type of neoplasm?

A

clear cell adenocarcinoma of the vagina

Precursor : vaginal adenosis (remant of cervical type glandular epithelium in vagina/mucosa)

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9
Q

what is the number one CLINICAL sx of hypercalcemia?

VS, #1 cause of INCIDENTAL finding of hyperparathyroidism?

A

MALIGNANCY:

1) osteolytic metastases (tumore –> cytokines –>ostelysis –> maturation of osteclasts)
2) paraneoplastic syndrome via PTH-related protein –> bone reabsorption

INCIDENTAL FINDING - probably primary hyperparathyroidism (#1- parathyroid adenoma)

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10
Q

What is the most common cause of primary hyperparathyroidism?

A

Parathyroid adenoma

Other causes: primary hyperplasia (diffuse or nodular), parathyroid carcinoma

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11
Q

Which MEN are associated with parathyroid?

A

MEN 1

(Parathyroid, pituitary and pancreas)

MEN 2 A

(parathyroid, pheochromocytoma, medullalry thyroid carcinoma)

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12
Q

Causes of hypercalcium with…

INC PTH

DEC PTH

A

Hypercal + INC PTH ==> hyperparathyroidism, familial hypocalciruic-hypercalcemia (FHH)– MEN1/MEN2A/FHH

Hypercal + DEC PTH ==> hypercalcemia of malignancy, vit D tox, immobilization, thiazide diuretics, granulomatous dz (sarcoidosis)

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13
Q

Cause of secondary hyperparathyroidism:

A

chronic dec/chronic low levels of calcium

primarily due to RENAL FAILURE (dec phsophate excretion –> hyperphso –> dec serum calcium –> parathyroid simulation

OR: renal mass –> dec alpha-1-ydroxylase –> dec active vitamin D –> parathyorid stimulation

others: dec dietary calcium, steatorrhea, vit d deficiency

SX: similar to 1

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14
Q

Causes and symptoms of HYPOparathyroidism:

A

DEC PTH and DEC calcium

causes: (rare), surgical removal, autoimmune, AD gain function of CASR, familial mutation at PTH precursor peptide, congenital absence of parathyroid - de george syndrome 22q11 (thymic absence)

SX: tetancy, chvostek sign, trousseau sign, mental status changes, intracranial manifestations, occular disease, qt elongation, dental abnormalities

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15
Q

MEN 1 = _____ of ___ chromosome

it is a ____gene.

MEN 2A, _____mutation at ____ gene ____ chromosome

FHH__ gene that causes a cahnge in __ receptor

A

MEN 1 = inactivation of 11q13,

tumor suppressor gene

MEN 2A = activating mutaiton of RET (10q), tyrosine kinase R, proto-onco gene

FHH = auto dominant, gain of function/increases sensistivity of parathyroid calcium sensing receptor gene (CaSR) on 3q

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16
Q

In osteoporosis:

Bone mass is [INC/DEC]?

Mineralization?

Histo?

What does the DEXA measure? What would classify osteoporosis?

A

In osteoporosis:

Bone mass is DECREASED

Mineralization- NORMAL

Histo: DEC bone trabecule, despite normal mineralization

Clinical: fractures (minimal trauma), vertebral fractures (loss of height, kyphoscoliosis, Dowager’s hump), pain, pulmonary embolism, pneumonia

Most common sites: humerus, spine, hip, distal radius

Dx: DEXA scan- measures bone thickness, density; WHO T score: Osteoporosis:BMD or BMC 2.5SD or more below the young adult mean

17
Q

How can a decrease in estrogen lead to osteoporosis?

A

DEC estrogen –> increase IL 1, IL 6, and TNF alpha by monocytes

DEC OPG

–> INC activity of osteoclast

18
Q

How do corticosteroids affect bone??

A

inhibits osteoblastic activity by suppressing their action can lead to secondary osteoporosis

19
Q

Rickets / Osteomalacia

How does it affect bone?

What is there an accumulation of?

What lab findings would you see?

A

Rickets/Osteomalacia:

Etiology = Vitamin D deficiency –> (vitamin D required for calcium / phosphate to mineralized osteoid laid down by osteoblast)

Bone mineralization defect

Accumulation of osteoid (unmineralized bone, soft bone)

DEC: vitamin D, calcium, phosphate, INC PTH, INC alk phos

20
Q

What is the effect of severe hyperparathyroidism on bone?

A

INC PTH –> INC resorption

osteoclast tunnel in –> dissecting osteitis

–> With continued microfractures and associated hemorrhages there is an influx of macrophages and ingrowth of reactive fibrous tissue which results in the development of mass lesions known as “brown tumors”

HALLMARK: osteitis fibrosa cystica von Recklinghausen disease of bone

21
Q

Lab findings in pagets?

A

ISOLATED ALK PHOS

everything else is normal

22
Q

Clinical findings of osteogenesis imperfecta?

A

Brittle bone disease

AUTO DOM defect in type 1 collagen

defect in extracellular structural protein

CLINCIAL:

  1. Multiple fractures- mimic child abuse (NO BRUISING)
  2. Blue sclera- thinning of scleral collagen reveals underlying choroidal veins
  3. Hearing loss- bones of the middle ear fracture easily
23
Q

Achondroplasia:

what is affected? …genetics?

Clinical presentation:

A

Path: impaired cartilage proliferation in the growth plate due to activating mutation in fibroblast growth factor receptor 3 (FGR3)- AD-

80% new mutations

Clinical: short extremities with normal-sized head and chest (dwarfism)- poor endochondral bone formation, intramembranous bone formation is not affected

24
Q

Osteoma:

typical location

what syndrome is associated with osteoma’s?

A

1.Benign tumor of bone

2.Commonly arises on the surface of facial bones

  • Tumor like mass of abnormally dense bone
  • Almost exclusively in the skull- paranasal sinus & facial bones
  • 4th-5th decade

3.Associated with Gardner Syndrome (osteomas, epidermal cysts, fibromatoses, and colonic adenomatous polyposis)

25
Q

Gardner Syndrome

Associated gene

A

APC (autosomal dominant)

Osteomas of the skull

  • Tumor-like mass of abnormally dense bone
  • Epidermal cysts
  • Fibromatoses
  • Thyroid Cancer
26
Q

multiple hereditary exostosis syndrome

A

AUTO DOM

EXT1 or EXT 2 genes

multiple osteochondromas develop in childhood. Patients may also have bowed, shortened bones. With respect to pathogenesis there are germline loss of function mutations in EXT1 or EXT 2 genes which result in defective enchondral ossification “setting the stage” for abnormal growth. Patients are at risk for the development of chondrosarcoma or other sarcomas.

27
Q

McCune-Albright Syndrome

A

McCune-Albright Syndrome - polyostotic fibrous dysplasia (multiple bones affected) + endocrinopathies such as precocious puberty, hyperthyroidism, pituitary adenomas secreting growth hormone and café-au-lait skin pigmentation (usually unilateral macular pigmented skin). Associated with mutations of the GNAS gene.

Recurrent fractures may lead to deformities of the lower extremities

28
Q

Where is the enzyme 11-b HSD1 and 2 expressed? What is their main function?

A

11b-HSD1 = liver, adipose tissue and brain

ACTIVATES a pro-drug (ie- cortisone —> cortisol)

one is simply activating

11b-HSD2 = kidney, salivary gland, colon

Inactivates a drug (ie- cortisol –> cortisone)

two to one is stepping down one so you are inactivating

29
Q

What affects does cortisol have on calcium?

A

decreases calcium absorption

–> in cortisol deficiency –> hypercalcemia [abd pain, n/v, anorexia]

30
Q

When would a HPA axis deficiency produce hyperpigmentation?

A

when the axis is working to INC teh ACTH –> INC of POMC gene –> MSH gene also gets produced = hyperpigmentation

primarily seen with primary adrenal insufficiency due to the lack of negative feedback on the anterior pituitary (lack of feedback INC POMC)

31
Q

What are some symptoms of primary adrenal insufficiency?

A

Impaired brain/kidney/heart fxn

hypotension

musc weakness

abd pain, N/V, anorexia

INC pigmentation

hypOnatremia:

Salt wasting/craving

Confusion

musc weakness

appetitie loss

dehydration

hyperkalemia:

cardiac arrythmia

musc wasting

malase

32
Q

How canyou assess whether you have overdosed a patient with cortisol?

A

Excessive Dosing: ­

weight gain, facial plethora, hypertension, euphoria

and other “__Cushingoid symptoms__”

33
Q

in a patient who suffers from adrenal insufficiency, when should you increase their hormone replacement treatment?

A

minor illness, surgery, pregnancy

34
Q

Which wart is associated with HPV?

A

Exophytic Condyloma
“Condyloma Acuminatum

35
Q
A

MSY2 Repro/Endo (7 decks)

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