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252 Cards in this Set

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Which hormones use cAMP as 2nd messenger?

FLAT chAMP GCG - FSH, LH, ACTH, TSH, Calcitonin, hCG, ACTH, MSH, PTH GHRH, CRH, Glucagon and V2 receptors

Which hormones use IP3 pathway?

GnRH, TRH, Oxytocin, Vasopressin (V1 receptors)

Steroid hormones have to be bound to "binding globulins" to make them more soluble (since they have to be lipophilic to be able to cross into cytoplasm where their receptor is)

Just know that

Amount of binding globulin available affects the amount of free hormone and activity of steroid hormones

eg pregnancy can increase sex hormone binding globulin and decrease amount of circulating testosterone

Anterior lobe forms from ____ and posterior lobe develops from _____

Rathke's pouch (ectodermal diverticulum),



hypothalamus invagination (neuroectoderm)

What does FSH act on in women? Men? What about LH?

FSH in women acts on granulosa cells and leads to follicular development.



In men it acts on sertoli cells to stimulate sperm maturation/development.



-----------------------------------------


LH acts on leydig cells in men to make testosterone.



In women acts on theca cells to make estrogen and progesterone (important for corpus luteum formation)

GnRH must be PULSATILE to stimulate FSH and LH release from anterior pituitary

Just know that

Inhibit inhibits....



Progesterone, Testosterone inhibit...

1. FSH



2. LH

Common alpha subunit between these 4 hormones

LH, FSH, TSH, hCG

In addison's disease, cortisol is low, so ACTH is high - why do you turn brown with this?

Because ACTH production is increased 
 
ACTH is synthesized as part of POMC (proopiomelanocortin) which contains sequences of other things including melanocyte stimulating hormones (MSH)

Because ACTH production is increased



ACTH is synthesized as part of POMC (proopiomelanocortin) which contains sequences of other things including melanocyte stimulating hormones (MSH)

What inhibits growth hormone

Somatostatin and feedback by IGF-1



NOTE: since Growth hormone doesn't have a downstream receptor -- it has a downstream hormone (IGF-1) that it activates



IGF-1 is what stimulates all the growth; it feeds back on growth hormone too

How can a prolactinoma cause secondary amenorrhea?



-----------------



Medical treatments of prolactinoma?

it decreases GnRH release from hypothalamus so decreased FSH/LH release



-----------------------


Bromocriptine, Cabergoline: DA agonists

TRH stimulates TSH and

prolactin

Growth hormone can cause impaired glucose tolerance and insulin resistance

So acromegaly patients often have diabetes

What is the screening test for acromegaly or gigantism (excess GH in kids)? What's the confirmatory test?



-----------------


GH is pulsatile -- when is it the highest?

IGF-1, then if high ....



Oral glucose tolerance test then check growth hormone (glucose normally supresses GH, but in acromegaly it won't)


-------------------------


GH is highest at night

Treatment of acromegaly (... and what other indications do we have for this drug)

tumor resection and octeotride (somatostatin analog)



----------------


Can also use SSA analogs to treat:


1. ZE syndrome, carcinoid syndrome, VIPoma, glucagonoma, insulinoma



2. Need to reduce splanchnic circulation: portal HTN (bleeding esophageal varices), bleeding peptic ulcers



Pituitary necrosis due to post partum bleeding and subsequent underperfusion of pituitary (agalactorrhea, hypothydroism, amenorrhea result)

Sheehan syndrome

Adrenal neuroblastoma vs pheochromocytoma

Adrenal neuroblastoma is in kids and has sustained hypertension (not episodic like pheo in adults)

This drug inhibits 5 alpha reductease to stop testosterone to DHT conversion.



What are its sid

finasteride

What happens if you have 3 beta hydroxysteroid dehydrogenase?

Can't make glucocorticoids, androgens, mineralocorticoids or estrogens - just have DHEA and progenolone buildup (precursors). Early death and a lot of salt wasting b/c no mineralocorticoids

If you have 17 alpha hydroxylase deficiency, what metabolite builds up? What sx do you have?

Deoxycorticosterone builds up, and you have just mineralocorticoid effect b/c of deoxycorticosterone (deficient sex hormones and glucocorticoids)

If you have 11 alpha hydroxylase deficiency, what builds up and what sx do you have?

You have deoxicorticosterone and 11 deoxycortisol. You still have androgns and mineralocorticoid effect, but low cortisol

If you have 21 alpha hydroxylase deficiency, what sx do you have and what builds up?

You have only androgens (early puberty, virillization) but no cortisol or mineralocorticoid effects. 17 hydroxyprogesterone builds up

Why is cortisol important? 4 basic sets of effects of cortisol are:

1. Maintain BP: uregulates alpha1 arteriole receptors to maintain BP



2. Increases energy substrates: Also increases gluconeogenesis, lipolysis, proteolysis



---> longterm use of steroids can therefore cause diabetes



3. Anti-inflammatory effects: suppresses immune system & inflammation



4. Decreases bone formation

Glucocorticoid antiinflammatory action

Inhibits COX and Phospholipase A2

4 causes of cushing syndrome

1. Exogenous steroid use (most common)



2. Cushing disease (ACTH producing pituitary adenoma)



3. Small cell carcinoma in lung making ectopic ACTH, or cortisol producing adrenal adenoma



4. (rare) cortisol-producing adrenal adenoma (see low ACTH here)

Dexamethasone results with cushing disease? Small cell carcinoma/ectopic? Cortisol producing tumor?

The only tumor that is suppressible is ACTH-producing tumor (specifically with high dose dexamethasone)

The only tumor that is suppressible is ACTH-producing tumor (specifically with high dose dexamethasone)

How can you tell the difference between ectopic ACTH (small cell cancer) and cortisol producing tumor since both of their dexamethasone supression tests will not suppress cortisol levels?

Measure ACTH - it'll be low in cortisol producing tumor (feeding back and decreasing ACTH), but in ectopic ACTH production, ACTH will be high

This synthetic mineralocorticoid is used for dangerously low aldo levels

Fludrocortisone

Primary hyperaldosteronism - aldo secreting adrenal tumor - what sx do you see?
 
 

Primary hyperaldosteronism - aldo secreting adrenal tumor - what sx do you see?



Conn syndrome. Will have LOW RENIN.
 
1. HTN (b/c of Na and water retention),
2. Hypokalemia b/c dumping K
3. metabolic alkalosis b/c dumping H

Conn syndrome. Will have LOW RENIN.



1. HTN (b/c of Na and water retention),


2. Hypokalemia b/c dumping K


3. metabolic alkalosis b/c dumping H

Primary vs secondary vs tertiary adrenal insufficiency

Primary -- problem with adrenal itself overproducing 
 
Secondary -- problem with anterior pituitary
 
Tertiary -- problem with hypothalamus

Primary -- problem with adrenal itself overproducing



Secondary -- problem with anterior pituitary



Tertiary -- problem with hypothalamus

Most common cause of Addison's disease (primary adrenal insufficiency)?

Autoimmmune destruction of adrenal cortex (80% of cases)



Symptoms of primary adrenal insufficiency?

Can't make cortisol, can't make aldosterone:



- Hypotension


- hyponatremia


- hyperkalemia


- fatigue, weight loss


- skin hyperpigmentation (b/c of POMC) -- ONLY a feature of primary adrenal insufficiency, not secondary or tertiary

Acute primary adrenal insuficiency due to adrenal hemorrhage

Waterhouse Friderichsen syndrome, associated with meningicoccal sepsis/DIC

Symptoms of secondary adrenal insufficiency?

No ACTH --> NO CORTISOL


But ALDO is still intact



Weakness, malaise, weight loss



BUT: NO hyperkalemia, NO hypotension, NO hyperpigmentation

Abrupt withdrawal of long term corticosteroids can cause

Tertiary adrenal insufficiency because steroids had been supressing CRH and if you don't taper it off you get this abrupt issue

Tertiary adrenal insufficiency because steroids had been supressing CRH and if you don't taper it off you get this abrupt issue

Chromaffin cells -- what is their function & what's their origin?

- Produce catecholamines in adrenal medulla



- Derived from neural crest origin (hyperplasia in pheochromocytoma)

Check serum for these metabolites in pheo

Metanephrine, normetanephrine, VMA - vanyllylmandelic acid



(these are the breakdown products of catecholamines)

What's the rule of 90's as it applies to pheochromocytoma?

- 90% are benign


- 90% are unilateral


- 90% are within the adrenal medulla


- 90% do not calcify


- 90% are seen in adults

Pheos are associated with

MEN 2A and 2B and neurofibromatosis I

How can a pheo cause polycythemia?



& what are the 4 tumors that can do this?

Can secrete EPO



Side note: what are the 4 tumors that can secrete EPO?



- Pheos


- RCC


- HCC


- Hemangioblastoma

Treatment for pheochromocytoma?


----------------



Why should you never give beta blockers alone for a pheo treatment?

1. Phenoxybenzamine -- alpha blocker


2. Beta blocker to further control tachycardia if necessary


3. Surgical resection


---------



Remember: pheos are releasing epinephrine --> which stimulate BOTH beta & alpha receptors



Blocking betas --> unopposed alpha1 --> increased vasoconstriction

Adrenal neuroblastoma:



1. associated oncogene?


2. Tumor marker?


3. Histologic finding?


4. Histochemical stain?

1. N-myc
2. Bombesin tumor marker
3. Homer Wright Pseudorosettes
4. Neurofilament stain

1. N-myc


2. Bombesin tumor marker


3. Homer Wright Pseudorosettes


4. Neurofilament stain

MEN1 tumors

Parathyroid adenomas,


pituitary adenoma,


pancreatic tumor (gastrinoma, insulinoma, glucagonoma, VIPoma) - the "THREE P's"



Common presenting signs:


- Hypercalcemia


- Stomach ulcers

MEN 2A

Medullary thyroid cancer,


pheo,


parathyroid hyperplasia

Men 2b

Medullary thyroid cancer, pheo, and mucosal neuromas

MEN 2A and 2B associated with this mutation

RET oncogene

Easy way to remember MEN 1, 2A, 2B

PPP (parathyroid, pituitary, pancreas)



PPM (parathyroid, pheo, medullary thyroid cancer)



PMM (Pheom, medullary thyroid cancer, Mucosal neuroma)

If thyroglossal duct doesn't disappear, what hapens?



-----------------------



Where is the most common ectopic thyroid tissue site?

The thyroglossal duct becomes the pyramidal lobe



----------------



The tongue is the most common ectopic tissue site


Once iodine is in thyroid, what happens to it?




---------------------------------------------



Thyroxinde-binding globulin is the protein that carries thyroid hormone in the blood. In which conditions is this protein low?

Organification - it's oxidized by peroxidase and then then forms thyroglobulin



--------------------



TBG is low in:


-Hepatic failure, nephrotic syndrome (low protein states)



--> This produces a low Total T3, T4; but FREE T3, T4 remain unchanged


This thyroid disease associated with HLA DR3 and HLA B8 and has a 4:1 female predominance

Graves disease

Increased radionucleotide iodine uptake in a diffuse pattern

Graves disease -- whole thyroid is soaking up as much iodine as it can to make all this excess thyroid, so radio nucleotide uptake is increased

Exopthalmus and pretibial myxadema

1. exopthalmus -- abnormal deposition of CT in the orbit



2. peritibal myxadema -- thickening of the skin on the front of the shins

Propylthiouracil and methimazole



- What are these drugs and their associated side effects?


- Use in maternal hyperthyroidism?



-------------------------------


Other treatment options?

PTU inhibits peroxidase enzyme to decrease thyroid hormone production and also decreases peripheral T4 to T3 conversion


-- S/E: liver dysfunction, agranulocytosis


---1st trimester use by mom



Methimazole - also inhibits peroxidase, but no peripheral function


---S/E: agranulocytosis, Fetal aplasia cutis (scalp defect in baby)


--- 2nd/3rd trimester use by mom & more commonly used for Graves in general



------------------------------------------



- Beta blockers


- Radioactive iodine or surgical resection; both w/ subsequent hormone replacement

Focal patches of hyper functioning follicular cells due to TSH receptor mutation -- the follicles functional independently of TSH



-----------------------------


What is the pattern seen in these diseases on RAI uptake?

Toxic multinodular goiter or toxic adenoma if just one



-----------------------



"Hot nodules"

Iodine induced hyperthyroidism

Jod Basedown phenomenon - hyperparathyroidism second to ingestion of iodine in any form:


- diet


- CT contrast administration


- amiodarone use

Focal destruction of thyroid w/ granulomatous inflammation



-Associated with HLA B35


-Often caused by viral infections

Subacute thyroiditis (de Quervain)

Subacute thyroiditis sx

-Painful/enlarged thyroid


-Acute febrile state


-NEGATIVE RAI uptake


-Hyperthyroid at first but if lasts long enough and destroys enough thryoid tissue, hypothyroid

Treatment of thyroid storm -- big surge of thyroid hormone & catecholamines

Beta blocker plus PUT/Methimazole

Hyperthyroidism due to teratoma

Struma ovarii teratoma - can have functional thyroid tissue in it

Low TSH, high T3/T4, but low iodine uptake on thyroid scan

Subacute thyroiditis or factitious hyperthyroidism

Levothyroxine

Synthetic analog of T4, side effects occur if patient takes too much -- these side effects look like hyperthyroidism

Cretinism aka ____. What are the symptoms of this?



congenital hypothyroidism:



Impaired physical growth, mental retardation, big tongue, big abdomen


Hypothyroidism with painless goiter


5:1 female predominance


MCC of hypothroidism in the U.S.

Hashimoto's - autoimmune disorder
Symptoms include:
 
 

Hashimoto's - autoimmune disorder


Symptoms include:



Cancer risk with hashimoto's?

B cell lymphoma

Fixed, hard, rock like, painless goiter.



Extension into airway common and obstructs it.



Histology shows fibrosis, macrophages, and eosinophils

Riedel's thyroiditis

Thyroid cancers are usually ____ nodules on scans (that's why we never do them)

cold

Benign thyroid nodules:



-Nodular Hyperplasia


-Follicular carcinoma



Describe the findings in each

Nodular Hyperplasia:


- Heterogenous appearance


- Cells surrounded by an INCOMPLETE capsule



Follicular carcinoma


- Thick, fibrous capsule


- Non-fixed mass that moves with swallowing

- Most common type of thyroid cancer
- Orphan annie eye nuclei (white looking), psammoma bodies
 
- Good prognosis

- Most common type of thyroid cancer


- Orphan annie eye nuclei (white looking), psammoma bodies



- Good prognosis

Papillary thyroid carcinoma

If papillary cancer is hereditary, associated with these mutations

RET gene or BRAF gene mutations

Cuboidal cells surrounded by fibrous capsule that this thyroid cancer often invades into
 
- Can even spread hematogenously

Cuboidal cells surrounded by fibrous capsule that this thyroid cancer often invades into



- Can even spread hematogenously

Follicular carcinoma

RAS mutation or PAX8-PPAR gamma 1 rearrangement mutation with this thyroid cancer

Follicular carcinoma

How do follicular adenoma and follicular carcinoma differ?

Both have capsules, but carcinoma invades the capsule

Proliferation of parafollicular C cells in thyroid secreting calcitonin



Associated w/ RET gene mutation, activation of tyrosine kinase receptor (like in papillary carcinoma)

Medullary carcinoma

Medullary thyroid carcinoma associated with

MEN 2a and 2b

In young patient with rock hard thyroid nodules, think ____. If older patient think ____

Riedel's thyroiditis, anaplastic thyroid carcinoma (bad prognosis)

Complications of thyroid surgery include

parathyroid removal/damage, damage to recurrent laryngeal nerves causing hoarseness

Pancreatic cells and their secretions - alpha, beta, delta cells

alpha make glucagon,


beta make insulin,


delta make somatostatin

C peptide is important to measure to differentiate between

Type 1 and Type 2 diabetes as well as causes of hypoglycemia (nurse injecting insulin into herself vs insulinoma)

Type 1 and Type 2 diabetes as well as causes of hypoglycemia (nurse injecting insulin into herself vs insulinoma)

Describe how glucose stimulates beta cells in pancreas to secrete insulin

First, glucose enters via GLUT 2, then it's metabolized down by glycolysis and that increases ATP levels. That causes ATP sensitive K channels to close, so K can't go out anymore and it depolarizes and causes voltage gated calcium channels to open...

First, glucose enters via GLUT 2, then it's metabolized down by glycolysis and that increases ATP levels. That causes ATP sensitive K channels to close, so K can't go out anymore and it depolarizes and causes voltage gated calcium channels to open, move into cell and that triggers insulin exocytosis from beta cells

GLUT-2 is insulin independent. Where is this found?



Glut-1 is also insulin independent, where is this found?



Glut 4 is insulin dependent, where is this found?

GLUT 2 found on beta cells of pancreas, liver, kidney, and small intestine.



Glut 1 found on RBCs and brain.



Glut 4 found on skeletal muscle and adipose tissue

Insulin receptor is a

tyrosine kinase.



Whereas Glucagon is a G protein receptor

Glutamic Acid decarboxylase (GAD) antibody in islet cells -- causes this condition.



List the classic symptoms associated w/ this condition

Type I diabetes:


- Hyperglycemia


- POLY uria, dipsia, phagia


- Weight loss

Two basic causes of complications in diabetes

Osmotic damage and non enzymatic glycosylation

Retinopathy, nephropathy, and vascular disease are complications of diabetes caused by

non enzymatic glycosylation



Retinopathy can be proliferative or non proliferative:



-Non-proliferative = leaky vessels


-Proliferative = formation of fragile new vessels in the eye --> can break and cause hemorrhages --> blindness



-Can also see soft exudates called "cotton wool spots"

Kimmelsteiel wilson nodules



----------



Can use these drugs to slow the rate of nephropathy

Acellular nodules in diabetic nephropathy on biopsy



--------------


ACEs, ARBs

Glucose is converted to sorbitol via ____ and sorbitol is converted to fructose via_____

aldose reductase, sorbitol dehydrogenase
 

aldose reductase, sorbitol dehydrogenase


Why does sorbitol cause damage to schwann cells, lens, retina, and kidney?



And what kind of damage is seen?

 
Because these cells don't have sorbitol dehydrogenase, so they can't convert sorbitol to fructose and it gets trapped there and causes osmotic damage to these tissues
 
 


Because these cells don't have sorbitol dehydrogenase, so they can't convert sorbitol to fructose and it gets trapped there and causes osmotic damage to these tissues



Describe pathogenesis of DKA causing dehydration and acidosis

Body doesn't have glucose, so a ton of glucagon is being stimulated to make glucose and that causes polyuria (since glucose can't actually go into cells) and leads to dehydration. Glucagon also breaks down fatty acids into ketones and that leads to profound acidosis

DKA patients often have HYPERkalemia - then why are we giving them potassium???

It's because H/K exchange with cells then we pee out all that K. So they look like they have elevated serum potassium but overall body potassium stores are LOW

It's because H/K exchange with cells then we pee out all that K. So they look like they have elevated serum potassium but overall body potassium stores are LOW

Sx of Hyperosmolar hyperglycemic state



Lab values as well

confusion/delirium/coma, severe dehydration, N/v, abdominal pain

confusion/delirium/coma, severe dehydration, N/v, abdominal pain

Primary mechanism of metformin? Side effects?

Decrease gluconeogenesis in the liver.



Side effects - GI upset or lactic acidosis in patients with renal dyfunction so don't give it to them

How do sulfonylureas work? What are these drugs to know? Side effects?

Glimepiride, glipizide, glyburide.
 
They block K channels on beta cells and depolarize the cell to cause Ca influx and stimulate insulin release.
 
Side effects: hypoglycemia and weight gain

Glimepiride, glipizide, glyburide.



They block K channels on beta cells and depolarize the cell to cause Ca influx and stimulate insulin release.



Side effects: hypoglycemia and weight gain

What are the TZDs and how do they work?



Side effects?

Pioglitazone and rosiglitazone - increase insulin sensitivity in peripheral tissues by binding to PPAR-gamma receptors.



This receptor regulates fatty acid storage and regulates glucose metabolism, decreases insulin resistance.



Rosi -- Weight gain and fluid retention (worsen CHF).



Pio -- Bladder cancer, hepatotoxicity!

Which diabetes drugs to avoid in patients with renal issues? Liver issues?

Metformin



Pio/rosiglitazone

What are the DPP-4 inhibitors and how do they work?

all end in ____gliptin.



DPP4 normally inhibits incretins, so if we inhibit the inhibitor, incretins aren't broken down as much and these things improve pancreatic function

Exanatide and Liraglutide are which class of diabetes drugs?

GLP-1 analogues - decrease glucagon secretion, increase insulin secretion, delay gastric emptying.



NO RISK FOR HYPOGLYCEMIA



S/E = increased risk for acute pancreatitis

Which diabetes drugs have lower risk of hypoglycemia and are good for old people so they don't fall and break their hips?

DPP-4 inhibitors and GLP-1 analogs (exentide and liraglutide)

Acarbose, miglitol - what are these drugs and what are their side effects?

alpha glucoside inhibitors - inhibit alpha glucosidase --> prevent sugar/starch digestion and decreases post prandial hyperglycemia.



S/E: Farting, diarrhea, cramping ,etc

Which hypothalamic nuclei are involved in hunger/satiety?

Remember the pneumonic - lesbian PDA involves Vaginas - Lateral hypothalamus, Paraventricular nuclei, Dorsal medial nuclei, arcuate nucleus, and ventromedial nuclei

Which hypothalamic areas are inhibited/stimulated by Leptin?

Lateral hypothalamus is inhibited by leptin when you're full, and if it's lesioned, you get anorexia. Ventromedial nuclei are STIMULATED by leptin, and this results in satiety. If destroyed, hyperphagia

When you're doing heavy exercise or your body is stressed, it needs more energy, so sympathetic drive (NE/E) activate adipocytes to

break down triglycerides to make fatty acids

Generally, what are the diagnostic criteria for metabolic syndrome?

Need 3 of these 5 -


big waist circumference,


high triglycerides,


high BP,


low HDL,


high fasting glucose

NASH looks just like alcohol fatty liver disease (NAFLD). What causes NASH?

Insulin resistance at liver (common with obesity/type 2 diabetes etc).



Excess lipid accumulates in liver and can progress to cirrhosis, HCC, or worsen Hep C progression

Chronically elevated LFTs in an overweight patient who doesn't drink

NASH

Weight loss drugs

Orlistat (but poop fat and that sucks), phentermine

Remember, PTH acts on osteoBLASTS, not osteoclasts directly

Blasts release RANK L and activates osteoclasts

Low magnesium decreases PTH SECRETION, WHAT 3 THINGS CAUSE LOW MAGNESIUM?

Diuresis, alcohol, aminoglycosides

PTH acts on kidneys to upregulate this enzyme

1 alpha hydroxylase to increase active vitamin D

1 alpha hydroxylase to increase active vitamin D

3 main functions of Vitamin D are:

1. increases dietary absorption of Ca


2. Increases dietary absorption of phosphate


3. Bone resorption of both Calcium and Phosphate

Which cancers cause increased PTHrP and hypercalcemia?

Squamous cell cancers (especially lung),


RCC


Breast metastasis to bone



NOTE: Multiple myeloma causes hypercalcemia as well


(But just through bone lysis, not PTHrP)

Excess vitamin D ingestion, Excess antacid ingestion (milk alkali syndrome) and granulmoatous diseases eg sarcoid or TB can cause

hypercalcemia

Which diuretics can cause you to become hypercalcemic? which ones can cause hypocalcemia?

Thiazides, loops

Signs and symptoms of primary hyperparathyroidism?

Stones, bones, abdominal groans, psychiatric overtones -


Renal stones,


osteosis fibrosa cystica/osteoporisis, osteomalacia/whatever,



constipation, peptic ulcers/indegestion, pancreatitis,



lethargy, fatigue, depression, psychosis/coma.

Secondary hyperparathyroidism common in patients with

chronic renal disease (can't make active vitamin D and can't absorb calcium in gut)- causing chronic hypocalcemia.
 
Body increases PTH to compensate for low calcium

chronic renal disease (can't make active vitamin D and can't absorb calcium in gut)- causing chronic hypocalcemia.



Body increases PTH to compensate for low calcium

How do primary and secondary hyperparathyroidism differ on labs?

Primary - high calcium, low phosphate, high PTH.



Secondary - low calcium, HIGH phosphate (b/c can't excrete it due to renal disease) and high PTH

Pseudohypoparathyroidism occurs when

Kidneys unresponsive to PTH - making plenty of PTH but kidneys can't respond to it



Albright Hereditary Dysplasia:


--Osteitis Fibrosa cystica


--Short stature, obesity, underdevelopment of 4th & 5th digits

Erection is due to parasympathetic stimulation via what nerve?

Pelvic nerve - nitric oxide here causes vasodilation and blood fills penis

Vagina muscles in wall cramp up when touched, and that's really painful, then they cramp more and become more painful. Vestibulitis is if you touch bartholin glands at opening of vagina and patients have a TON of bruning pain even though you're just touching (allodynia)

Prevents cGMP breakdown that leads to corpus cavernosum smooth muscle relaxation, so the vessels fill

Which nerve mediates the sympathetic response of sperm "emission" - where it moves from testes to the prostatic urethra?

hypogastric nerve

Which nerve involved with ejaculation?

Pudendal nerve - ejaculation is sympathetic!

Which ligament connects uterus, fallopian tubes, and ovaries to side wall? this ligament is ligated in hysterectomies

Broad ligament

Suspensory ligament connets the ovaries to the ____. The ovarian ligament connects the ovaries to the _____

Pelvic wall, uterus

Which ligament contains uterine vessels? Which one contains ovarian vessels?

Cardinal ligament, suspensory ligament of ovary

Vagina histo? Cervix histo? Fallopian tubes? Ovary?

Stratified squamous, simple columnar, ciliated columnar, simple cuboidal

Pudendal nerve block occurs at ischial spine, happens during deliveries often

Just know this

Why is a vericocele more common on left rather than right scrotum?

because right scrotom has less pressure b/c it brings blood RIGHT INTO IVC, left drains into left renal vein then IVC

Ovaries and testes lymphatic draining into

Para aortic lymph nodes

Indirect inguinal hernia and direct hernia - relationship to inferior epigastric artery. How about femoral hernias?

Indirect is lateral to this artery through inguinal ring. Direct hernia is MEDIAL to inferior epigastric artery through hesselbach's triangle (made up of inguinal ligament, lateral border of rectus abdominus, and inferior epigastric artery). FEMORAL HERNIAS below lignuinal ligament

Mesonephric duct goes on to become male genitalia if acted on by testosterone. Paramesonephric duct (mullerian) makes female genitalia unless inhibited by mullerian inhibiting factor

just know that

If two paramesonephric ducts don't fuse, what happens?

Bicornuate uterus - leads to infertility and stuff

SRY gene codes for

testis determining factor, which will make sertoli cells (which make MIF - mullerian inhibiting factor), Leydig cells - make testosterone (act on mesonephric ducts to make internal male genitals). Also makes 5 alpha reductase - converts testosterone to DHT which makes male external genitalia

What is exstrophy of the bladder? What congenital condition is it associated with?

Congenital gap in anterior bladder wall and abdominal wall infront of it.


Interior of bladder is open to outside world



-Associated w/ epispadias

Sertoli cells stimualted by ____. They secrete ____ , ____ and _____

FSH.


Stroll cells secrete:


1. MIF


2. Inhibin (decreases FSH)


3. ABP - androgen binding protein (which maintains level of testosterone in seminiferous tubules to help maturation of spermatogonia)

Finasteride what kind of drug? What do we use finasteride to treat?



---------------------


Flutamide is what kind of drug? What do we use flutamide to treat?

Finasteride slowly reduces DHT levels, used to treat BPH
S/Es: decreased libido, impotence, ejaculatory disorder


------------------


Flutamide is a competitive inhibitor at testosterone receptor and used in prostate cancer

Ketoconazole and spironolactone used in PCOS, how does each work?



S/Es of these 2 drugs?

Ketoconazole inhibits desmolase,


Spiro inhibits steroid binding



S/Es: gynecomastia, amenorrhea

Females with rudimentary vagina but 46 XY. Testes in labia majora



---------------



Androgen insensitivity - you don't have upper portion of vagina but you have lower portion, testes found in labia majora

Hypogonadic gonadism with olfactory bulb defect

Kallmann syndrome - female with primary amenorrhea or males with small testes

High riding testis with long axis oriented weirdly with absent cremasteric reflex

Testicular torsion

Failure of testis to descend into scrotum

Cryptorchidism

Testicular tumor with watery cytoplasm/fried egg appearance
 
(similar histologic appearance to oligodendrogliomas)
 
---------------------
Late mets & good prognosis

Testicular tumor with watery cytoplasm/fried egg appearance



(similar histologic appearance to oligodendrogliomas)



---------------------


Late mets & good prognosis

seminoma

Malignant tumor with painful, palpable mass in the scrotum and eleveated hCG
 
Histology is more glandular 

Malignant tumor with painful, palpable mass in the scrotum and eleveated hCG



Histology is more glandular

Embryonal carcinoma

Most common testicular cancer in children < 3
Elevated AFP, with schiller-duval bodies in testes (look like glomeruli)

Most common testicular cancer in children < 3


Elevated AFP, with schiller-duval bodies in testes (look like glomeruli)

Yolk sac tumor (aka aneodermal sinus tumor)

Lab values: Which tumors have increased...



1. AFP


2. hCG


----------------------------------------------------



Teratomas in males vs teratomas in females

1. AFP -- Yolk sac tumor


2. hCG -- choriocarcinoma, Embryonal carcinoma


----------------------------------------------------



Teratomas in males = MALIGNANT


Teratomas in females = benign

Testicular cancer,
Elevated hCG ,
tumor of trophoblasts,
can metastasize hematogenously 

Testicular cancer,


Elevated hCG ,


tumor of trophoblasts,


can metastasize hematogenously

Choriocarcinoma

Ranke crystals, androgen producing tumors of testes and can cause gynecomastia or percocious puberty

Ranke crystals, androgen producing tumors of testes and can cause gynecomastia or percocious puberty

Leydig cell tumor (a non-germ cell tumor)

These benign testicular tumors secrete estrogen and can cause gynecomastia, can be associated with puetz jeghers syndrome or carney syndrome

Sertoli cell tumors (a non-germ cell tumor)

Metastasis to testes, common in older men

testicular lymphoma

1. Fluid in scrotum due to incomplete fusion of processus vaginalis



---------------------


2. Dilated epididymal ducts

1. Hydrocele



---------------



2. Spermatocele

Dilated veins in pampiniform plexus and can cause infertility with "bag of worms" fealing in scrotom

Varicocele

Spermatocele

dilated epididymal duct

Greyish blue weird scap on genitalia that can progress to invasive squamous cell carcinoma in some patients

Greyish blue weird scap on genitalia that can progress to invasive squamous cell carcinoma in some patients

Bowen's disease

Angulation/bent penis, painful erections

Peyronie disease - due to inflammation and fibrous tissue formation of tunica albuginea

Prostatitis in younger man?



Older man?

Young people - think chlamydia/gonorrhea (sexual),



Older think UTI bugs (ecoli, kelbsiella, proteus, enterobacter).



Tx older people with fluoroquinolones and TMP/SMX

How does prazosin/doxazosin/terazosin help with BPH?



Side effects of these drugs?


--------------------------------



What is tamulosin?

relaxes prostate smooth muscle and improves urine flow



S/Es: Dizziness, postural hypotension, fatigue


---------------------------


Selective alpha1AD blocker



Fewer side effects than the -osins (nonselective alpha1 blockers)



Tamulosni does not affect the alpha1b receptors in blood vessels so you get NO antihypertensive effect

Where does prostate cancer metastasize to commonly? How do you treat it?

Bone (you'd see increased alk phos).



Treat with flutamide/resections



--Flutamide is a testosterone receptive competitive antagonist

Estrone vs estradiol vs estriol



Remember the 1 + 2 = 3 (man + woman = baby)

Estrone is made in periphery by fat cells via aromatase.



Estradiol - made in ovaries, abundant in women and gives women female characteristics.



Estriol found in placenta

Which two layers of endometrium are shed during menstruation?

Stratum compactum and stratum spongiosum (but stratum basalis stays)

Stratum compactum and stratum spongiosum (but stratum basalis stays)

What is mittelschmerz?

Mid cycle pelvic pain associated with ovulation; caused by peritoneal irritation caused by serous fluid release

Primary oocytes (diploid) arrested in ____


--------------------------------------------------------


Seconary oocytes (haploid) arrested in ____

Prophase I until ____. ovulation
 
Metaphase II until
("egg MET sperm"

Prophase I until ____. ovulation



Metaphase II until


("egg MET sperm"

Hormonal birth control supresses ovulation (because no LH surge occurs) and thickens cervical mucus (progesterone) and thins endometrium (progesterone)

just know that

Avoid OCPs in these women

Patients with history of clot/stroke, smokers > 35, or those who have migraines with auras

Clear cell adenocarcinoma of vagina with anatomic abnormalities of genital tract due to in utero exposure to

DES - diethylstilbestrol

This form of birth control is associated with bone mineral density loss, especially long term

Medroxyprogesterone (depo-provera IM shot)

IUDs are contraindicated in these patients

STDs - because you can push the infection into the wall and cause it to spread

Which vaginal wall tears correspond to a cystocele? Rectocele? Enterocele?

(1) anterior wall, bladder bulges into vagina - cystocele. (2) Posterior wall - rectum bulges through - rectocele. (3) Tear at tope of vagina - small intestines bulge through, that's an enterocele

What is vaginismus? what is vestibulitis?

Vagina muscles in wall cramp up when touched, and that's really painful, then they cramp more and become more painful. Vestibulitis is if you touch skene ducts or bartholin glands at opening of vagina and patients have a TON of pain even though you're just touching (allodynia)

Balloon/ball of inflammation at opening of vagina?

Balloon/ball of inflammation at opening of vagina?

Bartholin duct or skene duct cyst



What do these glands do? -- vaginal lubrication production

VIN?


VAIN?

Vulvar and vaginal intraepithelial neoplasia - very similar to CIN (all of these are pre-cancerous) but vulvular or vaginal. Associated with HPV (16, 18, 31, 33)

HPV genes that can cause cancer?

E6 and E7.
 
E6 - degrades p53, E7 inhibits Rb
 

E6 and E7.



E6 - degrades p53, E7 inhibits Rb


What do you see on histology for CIN/VIN/VAIN?

Koilocytes - look like a fried egg like oligodendrocytes
 

Koilocytes - look like a fried egg like oligodendrocytes


Vaginal cancer in girls < 4,
 
with spindle shaped cells and "grape like" appearance of tumor in vagina.
 
Also has positive desmin stain
-------------------------------------------------
Associated w/ DES (synthetic estrogen) exposure in utero

Vaginal cancer in girls < 4,



with spindle shaped cells and "grape like" appearance of tumor in vagina.



Also has positive desmin stain


-------------------------------------------------


Associated w/ DES (synthetic estrogen) exposure in utero

Sarcoma botryoides - these arise from bladder or vaginal wall



-------------------------------------


Clear cell adenocarcinoma of the vagina

How does cervical cancer spread? What changes can you see w/ advanced disease?

- Spreads locally



- Clinically staged



- Lateral invasion can block ureters, leading to renal failure

Endometrial tissue found outside uterus?


---------------------------------------------------------



Chocolate cysts, severe pain related to menstruation

Endometriosis



---------------------------------



Endometrioma or endometriosis in general

Theories for endometriosis pathogenesis?

Retrograde menstrual flow, hematologic/lymphatic spread,


direct spread,


or metaplasia

Tx for endometriosis

1. OCPs


2. Leuprolide (continuous GnRH agonist) as well 3. Danazol - mild androgenic medication to counteract estrogen and supress endometrial tissue

Endometrial tissue found within myometrium? What is this and what would you see on histology?

Adenomyosis - smooth muscle with endometrial glands inside of it on histology

Benign smooth muscle tumor in uterus that is estrogen sensitive and have a whorl pattern on histology?
 
-Increased rates in black women
 
-Stain positive for design

Benign smooth muscle tumor in uterus that is estrogen sensitive and have a whorl pattern on histology?



-Increased rates in black women



-Stain positive for design

Leimyoma (fibroid)



-Either asymptomatic or can cause bleeding

Tx for leimyomas? aka fibroids

OCPS, leuprolide (continuous GNRH analog), ablation or hysterectomy



Bulky, irregular shaped tumor with areas of necrosis and hemorrhage in uterus



Arises de novo



increased rates in black females



also stains positive for desmin stain

Leiomyosarcoma

LH acts on theca cells to make ____ via _____ (enzyme). This product crosses over into granulosa cells through the basement membrane.  
 
In the granolas cells, aromatase converts it to estradiol when activated by FSH

LH acts on theca cells to make ____ via _____ (enzyme). This product crosses over into granulosa cells through the basement membrane.



In the granolas cells, aromatase converts it to estradiol when activated by FSH

Makes androstenedione from cholesterol via desmolase

Diagnostic criteria for PCOS

2 of the following 3 are necessary for diagnosis
 
- oligo/anovulation
- hyperandrogenism,
- polycystic ovaries on ultrasound

2 of the following 3 are necessary for diagnosis



- oligo/anovulation


- hyperandrogenism,


- polycystic ovaries on ultrasound

Increased LH/FSH ratio

PCOS



1. LH stimulates theca cells to make androgens (that's why you get hirsutism)



2. That stimulates estrogen production from granulosa cells (which feed back and inhbit FSH production) - that's why your ratio is greater (LH/FSH)



----------------



ANVOLUTION results from the dysregulation of these hormones

Insulin resistance and obesity are also involved with PCOS - one of the mainstays of treatment is weight loss and metformin.



What do you use to treat hirsutism and estrogen overload?

Spironolactone and OCPs or progesterone, or leuprolide in pulsatile fashion

Clomiphene -- what's it used for? What's its mechansim of action?



Side effects?

Clinical use: anovulation, PCOS



MOA: Partial agonist at estrogen receptors in the hypothalamus --> relatively decreases the negative feedback of estrogen, therefore increases FSH



Side effects: hot flashes, vision changes, ovarian hyperstimulation & enlargement

CA-125

marker for ovarian cancer, but not specific, so mainly used to monitor disease

Gene mutations associated with family history of ovarian cancer?



What are some additional risk factors?

BRCA1, 2, and lynch syndrome



- Uninterrupted ovulatory cycles


- Nulliparity

What are the 4 categories of ovarian tumors?

Epithelial, germ cell, stromal, and metastatic

What are the types of epithelial ovarian tumors?

Serous, mucinous, endometrioid, clear cell, Brenner, mixed

Benign ovarian tumor/cyst lined by fallopian tube (ciliated) epithelium

Serous cystadenoma

Malignant ovarian tumor with psammoma bodies

serous cystadenocarcinoma

Ovarian tumor with cells that look like intestine, filled with mucine

mucinous cystadenoma or cystadenocarcinoma

Pseudomyxoma peritonei

This is intraperitoneal mucinous material that characterizes mucinous cystadenocarcinoma, also seen with cancers of the appendix

Ovarian tumor that's benign, solid, encapsulated, and looks like transitional epithelium of the bladder with "coffee bean" nuclei

Ovarian tumor that's benign, solid, encapsulated, and looks like transitional epithelium of the bladder with "coffee bean" nuclei

Brenner tumor

What are the ovarian germ cell tumors?

teratoma, dysgerminoma, endodermal sinus (yolk sac), and choriocarcinoma

Teratoma in patients with hyperthyroid? Are teratomas in females benign or malignant? What about males?

Struma ovarii teratoma - can have functional thyroid tissue in it



- Teratomas in men = malignant


- Teratomas in women = benign

Ovarian tumor equavalent of seminoma in males.



Made of undifferentiated germ cells - "sheets of uniform cells".



May produce LDH and hCG and associated with Turner syndrome

Dysgerminoma

Elevated AFP, with schiller-duval bodies in ovaries (look like glomeruli)



---------------------



Common site of mets for choriocarcinomas?

Yolk sac tumor aka endodermal sinus tumor



----------------------------------



Lung

What are the three types of stroma/sex cord ovarian tumors?



------------------------------------




Fibromas, granulosa-theca cell, sertoli-leydig cell



---------------------


Sertoli-leydig tumor details:



-Rare, large


-Contain testicular structures that produce androgens --> virilization



Meig's syndrome

Fibroma (benign ovarian tumor),


ascities (fluid in abdominal cavity), and


pleural effusion (hydorthorax)

Call exner bodies - eosinophilic fluid-filled spaces between granulosa cells
 
Further clues:
malignant, secretes  estrogen/progesterone/inhibin 
 
-can cause endometrial hyperplasia or percocious puberty

Call exner bodies - eosinophilic fluid-filled spaces between granulosa cells



Further clues:


malignant, secretes estrogen/progesterone/inhibin



-can cause endometrial hyperplasia or percocious puberty

Granulosa cell tumor

Musin-secreting signet ring cells in ovaries

Musin-secreting signet ring cells in ovaries

Krukenberg tumor metastasizing from GI (gastric cancer usually)

Cytotrophoblasts and syncytiotrophoblasts - what do they do?

They are the fetal component of the placenta.



Cytotrophoblasts are the inner layer and contain stem cells.



The syncytiotrophoblasts make bHCG and they're the outer layer, important for nutrient and waste transmission

Decidua basalis

Base layer of endometrium making up the maternal component of the placenta

What is the urachus? What happens if it doesn't close?

Connects fetal bladder to yolk sac. If it doesn't close you can have urine coming out of belly button, or outpouching of bladder into it

What is the vitelline duct? What happens when it doesn't obliterate?

Connects fetus midgut to yolk sac. If it doesn't obliterate, you get meckel diverticulum or a fistula to the belly button

Trisomy 21 vs Trisomy 18 on quad fetal screening (AFP estriol and hCG - which ones are low and high in each?




------------------


Side note... what is the mCC of abnormal serum screening?

In trisomy 18 - ALL ARE LOW



In trisomy 21, hCG is high, AFP & estriol are low


---------------------



MCC of abnormal serum screening is incorrect dating

What would you see on quad screen (fetal testing) with neural tube defects, abdominal wall defects, or multiple gestations (twins)?

Increased AFP

Twin-twin transfusion syndrome happens when twins share a placenta - what is this?

Anastamosis leads to shunting of blood - donor baby is anemic, pale, growth restricted. Recipient baby has polycythemia, fatter, and has heart failure

Edmeatous/grapelike chorionic villi are the buzzword for

Edmeatous/grapelike chorionic villi are the buzzword for

hydatiform mole pregnancy

Complete vs partial hydatiform mole pregnancy

Complete: 46xx or 46xy


- REALLY REALLY HIGH hCG


- Large uterus



Partial : 69xxy or xxx or xyy


- not as high hCG


- normal uterine size


- can have some fetal parts


- lower risk of choriocarcinoma or malignant trophoblastic disease

Early uterine rupture is pathognumonic for

Complete mole pregnancy

"honeycomb" or "snowstorm" appearance of uterus on ultrasound

Mole pregnancies

what is placenta previa?



What's the worst type? How does this present and what's the "cure"?

 
It's abnormal placement of the placenta.
 
Placenta attaches over or near the cervix so we can get a "preview" of the placenta in the cervical os
 
Complete is the worst, where it covers the cervix completely and baby can't be delivered throu...


It's abnormal placement of the placenta.



Placenta attaches over or near the cervix so we can get a "preview" of the placenta in the cervical os



Complete is the worst, where it covers the cervix completely and baby can't be delivered through there - so have to do C section.



Mom's present with painless vaginal bleeding

What is vasa previa?

fetal blood vessels covering cervix - massive risk of fetal hemorrhage if these tear

Painful vaginal bleeding in third trimester

placental abruption - trauma/smoking/cocaine increase risk of this happening

Why is fetal esophogeal or duodenal atresia associated with polyhydramnios?



Why is renal agenesis or posterior urethral valves associated with oligohydramnios?



------------------------------------------------------



Important association w/ polyhydramnios is:

Normal flow of amniotic fluid goes out of the baby (pee) and is swallowed by the baby, so if you have esophogeal issues or atresia, you can't swallow it and it builds up.



If you can't pee it out, you have oligohydramnios



----------------------------------------------------



Maternal diabetes is a huge predisposing risk factor for polyhydramnios


Oligohydramnios, limb/facial deformities, and pulmonary hypoplasia

Potter syndrome

Diagnostic criteria for preeclampsia? For eclampsia?

Preeclampsia - hypertension and proteinuria. Eclampsia = preeclampsia + seizures



----> see edema in face & upper extremities! (not diagnostic criteria, but a good tip)

What is HELLP syndrome?

**COULD SEE FIBRINOID NECROSIS IN PLACENTA VESSELS**

**COULD SEE FIBRINOID NECROSIS IN PLACENTA VESSELS**

Treatment for eclampsia? Side effects of this treatment?


Deliver baby and give IV magnesium sulfate for seizure risk




S/Es of Mg:


- Decreased DTRs


- Pulmonary edema


- Altered mental status


- Cardiac conduction defects

Pathogenesis of gestational diabetes?



First line drug for gestational diabetes?



-------------------------------------------------------------


Type I or Type II diabetes while pregnant are associated w/ which fetal anomalies?

HPL - human placental lactogen - this is physiologically important because it increases maternal insulin resistance to leave more glucose in blood for baby, but when this is extreme, you get gestational diabetes.



Baby can have macrosomia and risk of stillbirth



First line -- try weight loss. Then use insulin



-------------------------------------


- Congenital heart defects -- transposition of the great vessels


- Neural tube defects


- Caudal regression syndrome -- poor formation of the lower spine w/ problems in bladder control

Positive hCG, abdominal pain like appendicitis during first trimester and vaginal bleeding

Ectopic pregnancy -- where is most common location?



Fallopian tube



Symptoms?



- Occurs in 1st trimester


- Positive hCG


- Abdominal pain (b/c of bleeding)



Risk factors? ... anything that can cause scarring


- Infertility


- Salpingitis, PID


- Ruptured appendix


- Endometriosis


- Prior tubal surgery

Categories A, B, C, D, and X of drugs in pregnancy

A - safe.


B - presumed safety based on animal studies.


C - no studies show adverse effect,


D - human risk but benefits may outweigh risk,


X - contraindicated, risk clearly outweights benefits

Diseases in pregnancy and medications we use to treat -


(1) Hypertension


(2) Diabetes


(3) Epilepsy


(4) Hyperthyroidism


(5) Anticoagulation

(1) Hyertension - methyldopa, hydralazine, labetalol



(2) Diabetes - insulin



(3) Epilepsy - AVOID VALPROIC ACID, but can use anything else but supplement with increased folic acid to prevent neural tube defects



(4) Hyperthyroidism - PTU in 1st trimester, MMU in 2nd/3rd



(5) Anticoagulation - heparin or enoxaparin

Tocolytics are used to delay pregnancy - what are these?



Which drugs do we usually give with these drugs?

Indomethicin (cox inhibitor preventing stimulatory PGE formation),



Nifedipine - calcium channel blocker causes myometrial relaxation



Terbutaline, Ritrodine - B2 agonist on uterus and relaxes myometrium



Magnesium sulfate for seizure prophylaxis



--------


Give GCs (betamethasone, dexamethasone) to help increase fetal lung development

What do you use to promote labor in somebody to help with contractions/cervical dilation?

Prostaglandin anologs - dinoprostone, misoprostol and oxytocin

Mifepristone - this is used in medical abortions with 2 other drugs - name those drugs and the mechanisms of action of all of them

Synthetic steroid that's a competitive inhibitor of progesterone receptors



Used for abortions in addition to misoprostol (makes you contract) and methotrexate

name the teratogenic properties of these drugs (1) Ace inhibitors,


(2) aminoglycosides (eg gentamicin),


3 - Fluoroquinolones,


4- tetracyclines,


5- chlormphenicol,


6 - valproic acid,


7 - lithium,


8 - isotretinoin,


9 - DES (diethylstilbestrol),


10 - statins,


11 - thalidomide (used to treat multiple myeloma and other cancers)

1) Ace inhibitors - renal malformations, (2) aminoglycosides (eg gentamicin - ototoxicity ), 3 - Fluoroquinolones - cartilage damage, 4- tetracyclines - discolored teeth , 5- chlormphenicol - gray baby syndrome, 6 - valproic acid - neural tube defects , 7 - lithium - ebstein anomaly, 8 - isotretinoin - spontaneous abortion or really bad birth defects (category X) , 9 - DES (diethylstilbestrol) - vaginal clear cell adenocarcinoma 10 - statins - CNS/limb defects 11 - thalidomide - limb defects ,

Which drugs can cause gynecomastia?

Some Drugs Cause Awesome Knockers -


Spiro


Digoxin


Cimetidine


Alcohol (chronic)


Ketoconazole

Non-proliferative breast changes can either be

Fibrosis - hyperplasia of breast stroma, or cysts (aka "blue dome cysts" - fluid filled)

Caffeine and dietary fat can cause benign proliferative changes in breasts

just know that

Proliferative, benign, increased acini and intralobular fibrosis and calcifications without atypia in breast tissue

Sclerosing adenosis

Complex sclerosing lesion with radial scar on mammogram

Looks like fat necrosis, scar with irregular shape, but it's benign but proliferative

What are the three benign breast tumors to know?

Fibroadenoma,


Intraductal papilloma,


Phylllodes tumor

Small, firm breast tumor with regular edges.


Mobile, common in women under 25, and increases in size with estrogen exposure

Fibroadenoma - NOT a precursor for breast cancer

Small breast tumor, benign (but small cancer risk) found inside of lactiferous ducts, and causes serous/bloody nipple discharge

Intraductal papilloma

Large benign bulky tumor of the breast with leaf like projections on histology

Phyllodes tumor

Most important prognostic factor of breast cancer?

Lymph node involvement

Two general types of breast cancer?

Ductal - arises from duct epithelium, Lobular - arises from lobules (glands)

DCIS - ductal carcinoma in situ - what are the subtypes?


-------------------------------------



What is the characteristic finding of DCIS on mammography?

(1) Comedocarcinoma - caseous necrosis, solid, cribiform, papillary, micropapillary



----------------------------


Dystrophic calcification

Eczema-like patches on nipple and areola suggesting underlying carcinoma

Paget disease of breast - assocated with UNDERLYING DCIS

Signet ring cells in this breast cancer.



These cancers are ALWAYS ER+ and PR +



Relatively lower risk of progression to invasive carcinoma

LCIS - lobular carcinoma in situ

MC type of invasive breast cancer


- Firm, rock hard, immobile breast mass with sharp margins, often arises from DCIS

Invasive ductal carcinoma

Generally multiple & bilateral


Inactivation of E-cadherin genes,


ER+ and PR+ breast cancer,


and also has signet ring cells

invasive lobular carcinoma

What is tamoxifen? How does it work?



Tamoxifen activity in breast tissue vs endometrial tissue?

Tamoxifen = selective estrogen receptor modulators (SERMs)



- Antagonist at ER in breast,


- Agonist in endometrial tissue, so increases risk of endometrial cancer

Alternative to tamoxifen - estrogen agonist in bone, antagonist in breast, and does NOT cause increased endometrial cancer risk

Raloxifene

Anastrozole is also used to treat breast cancer - how does this work? Who is it commonly used in and what side effect is it assocaited with?

Inhibits aromatase -- thus inhibiting production of estrogen



Used in post menopausal women with breast cancer.



Side effect - osteoperosis due to antagonistic effect on bones

MC breast tumor in women under 25

Fibroadenoma

MC breast mass in postmenopausal women

Invasive Ductal Carcinoma

MC breast mass in premenopausal women

Fibrocystic change of the breast

Loss of e-cadherin adhesion gene on chromosome 16

Invasive lobular carcinoma