Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
171 Cards in this Set
- Front
- Back
|
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
All anterior pituitary hormones and some hypothalamic ones |
|
|
Which hormones use IP3 pathway? |
GnRH, TRH, Oxytocin, Vasopressin (V1 receptors) - Two from hypothalamus and the 2 posterior pituitary ones |
|
|
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, and in women acts on theca cells to make estrogen and progesterone (important for corpus luteum formation) |
|
|
Common alpha subunit between these 4 hormones |
LH, FSH, TSH, hCG |
|
|
TRH stimulates TSH and |
prolactin |
|
|
What is the screening test for acromegaly or gigantism (excess GH in kids)? What's the confirmatory test? |
IGF-1, then if high, oral glucose tolerance test then check growth hormone (glucose normally supresses GH, but in acromegaly it won't) |
|
|
Adrenal neuroblastoma vs pheochromocytoma |
Adrenal neuroblastoma is in kids and has sustained hypertension (not episodic like pheo in adults) |
|
|
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 |
|
|
4 causes of cushing syndrome |
exogenous steroid use (most common), Cushing disease (ACTH producing pituitary adenoma), Small cell carcinoma in lung making ectopic ACTH, or cortisol producing adrenal adenoma |
|
|
Dexamethasone results with cushing disease? Small cell carcinoma/ectopic? Cortisol producing tumor? |
Low dose will not suppress cortisol, but high dose will. In the other two, high dose will not change cortisol levels. |
|
|
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? |
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? |
Conn syndrome. Will have LOW RENIN. This is hypertension (b/c of Na and water retention), hypokalemia b/c dumping K, and metabolic alkalosis b/c dumping H |
|
|
Most common cause of addison's disease? |
Autoimmmune destruction of adrenal cortex |
|
|
Sx of primary adrenal insufficiency? |
Hypotension, hyponatremia, hyperkalemia, skin hyperpigmentation (b/c of POMC), low weight |
|
|
Sx of secondary adrenal insufficiency? |
Weakness, malaise, weight loss, but NO hyperkalemia, NO hypotension, NO hyperpigmentation (aldo is still being activated by RAAS) |
|
|
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 |
|
|
Pheos are associated with |
MEN 2A and 2B and neurofibromatosis I |
|
|
N-myc oncogene, bombesin tumor marker, neurofilament stain, and homer wright pseudorosettes associated with this adrenal cortex tumor |
Adrenal neuroblastoma |
|
|
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? |
Ectopic thyroid tissue in tongue |
|
|
Once iodine is in thyroid, what happens to it? |
Organification - it's oxidized by peroxidase and then then forms thyroglobulin |
|
|
This thyroid disease associated with HLA DR3 and HLA B8 |
Graves disease |
|
|
Propylthiouracil and methimazole - what are these drugs and their associated side effects? Which one of these is used in maternal hyperthyroidism? |
PPU inhibits peroxidase enzyme and decreases thyroid hormone production and also dcecreases T4 to t3 conversion. Methimazole - also inhibits peroxidase. Both can cause agranulocytosis but PPU can cause liver dysfunction too. Fetal aplasia cutis (scalp defect in baby), so PPU is used in pregnant moms during 1st trimester only but MMU is prefered in 2nd/3rd trimester). Beta blockers and radioactive iodine also used for hyperthyroidism |
|
|
Iodine induced hyperthyroidism - what can cause this besides diet? |
Jod Basedown phenomenon - diet or CT or amiodarone |
|
|
Focal destruction of thyroid granulomatous inflammation, associated with HLA B35, often caused by viral infections |
subacute thyroiditis |
|
|
Subacute thyroiditis sx |
Painful/enlarged thyroid, hyperthyroid first but if lasts long enough and destroys enough thryoid tissue, hypothyroid |
|
|
Treatment of thyroid storm |
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 |
|
|
Cretinism aka ____. What are the symptoms of this? |
congenital hypothyroidism. Impaired physical growth, mental retardation, big tongue, big abdomen |
|
|
Cancer risk with hashimoto's? |
B cell lymphoma |
|
|
Fixed, hard, rock like, painless goiter. Extention into airway common and obstructs it. Histology shows fibrosis, macrophages, and eosinophils |
Riedel's thyroiditis |
|
|
Orphan annie eye nuclei (white looking), psammoma bodies |
Papillary cancer |
|
|
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.
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 |
Medullary carcinoma |
|
|
In young patient with rock hard thyroid nodules, think ____. If older patient think ____ |
Riedel's thyroiditis, anaplastic thyroid carcinoma (bad prognosis) |
|
|
Pancreatic cells and their secretions - alpha, beta, delta cells |
alpha make glucagon, beta make insulin, delta make somatostatin |
|
|
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, 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 |
|
|
Glutamic Acid decarboxylase (GAD) antibody in islet cells |
Type I diabetes |
|
|
Glucose is converted to sorbitol via ____ and sorbitol is converted to fructose via_____ |
aldose reductase, sorbitol dehydrogenase |
|
|
Describe pathogenesis of DKA causing dehydration and acidosis |
Since you don't have insulin, your cells don't get 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 |
|
|
Sx of Hyperosmolar hyperglycemic coma/state |
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 function 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. 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. Weight gain and fluid retention (worsen CHF). AVOID IN PATIENTS WITH LIVER PROBLEMS |
|
|
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 |
|
|
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. 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 |
|
|
Generally, what are the diagnostic criteria for metabolic syndrome? |
Need 3 of these 5 - big waist circumference, high triglycerides, high BP, low HDL, and higher faster 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 - looks like NAFLD (alcoholic fatty liver disease). Caused by 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 |
|
|
Weight loss drugs |
Orlistat (but poop fat and that sucks), phentermine |
|
|
Low magnesium decreases PTH SECRETION, WHAT 3 THINGS CAUSE LOW MAGNESIUM? |
Diuresis, alcohol, aminoglycosides |
|
|
Which cancers (not just lung cancers) cause increased PTHrP and hypercalcemia? |
Squamous cell cancers (especially lung), renal cell carcinoma, breast metastasis to bone and multiple myeloma (But just through bone lysis, not PTHrP) |
|
|
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. |
|
|
Pseudohypoparathyroidism occurs when |
Kidneys unresponsive to PTH - making plenty of PTH but kidneys can't respond to it |
|
|
Erection is due to parasympathetic stimulation via what nerve? |
Pelvic nerve - nitric oxide here causes vasodilation and blood fills penis |
|
|
How does Siladenfil work? |
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 |
|
|
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 |
|
|
Exstrophy of the bladder |
congenital gap in anterior bladder wall and abdominal wall infront of it. Interior of bladder is open to outside world |
|
|
Sertoli cells stimualted by ____. They secrete ____ , ____ and _____ |
FSH, secrete MIF and Inhibin (decreases FSH) and ABP - androgen binding protein (which maintains level of testosterone in seminiferous tubules) |
|
|
Finasteride is used to treat ____. Flutamide is used to treat _____ |
BPH. Flutamide is a competitive inhibitor at testosterone receptor and used in prostate carcinoma |
|
|
Ketoconazole and spironolactone used in PCOS, how does each work? |
Ketoconazole inhibits desmolase, spiro inhibits steroid binding |
|
|
Testicular tumor with watery cytoplasm/fried egg appearance |
seminoma |
|
|
Malignant tumor with painful, palpable mass in the scrotum and eleveated hCG |
Embryonal carcinoma |
|
|
Most common testicular cancer in children < 3 |
Yolk sac tumor (aka aneodermal sinus tumor) |
|
|
Elevated AFP, with schiller-duval bodies in testes (look like glomeruli) |
Yolk sac tumor |
|
|
Ranke crystals, androgen producing tumors of testes and can cause gynecomastia or percocious puberty |
Leydig 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 |
|
|
Fluid in scrotum due to incomplete fusion of processus vaginalis |
Hydrocele |
|
|
Spermatocele occurs due to dilated |
dilated epididymal duct |
|
|
Greyish blue weird scab 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? |
relaxes prostate smooth muscle and improves urine flow |
|
|
Where does prostate cancer metastasize to commonly? How do you treat it? |
Bone (you'd see increased alk phos). Treat with flutamide/resections |
|
|
Estrone vs estradiol vs estriol |
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) |
|
|
Primary oocytes (diploid) arrested in Prophase I until ____. Seconary oocytes (haploid) arrested in metaphase II until ____ |
ovulation, fertilization |
|
|
Hormonal birth control supresses ovulation (because no LH surge occurs) and thickens cervical mucus (progesterone) and thins endometrium (progesterone) |
just know that |
|
|
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 top 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? |
Bartholin duct or skene duct cyst |
|
|
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) |
|
|
What do you see on histology for CIN/VIN/VAIN? |
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 |
Sarcoma botryoides - these arise from bladder or vaginal wall |
|
|
Chocolate cysts, severe pain related to menstruation |
Endometrioma or endometriosis in general |
|
|
Tx for endometriosis |
OCPs and Leuprolide - continuous GnRH agonist, as well as 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? |
Leimyoma |
|
|
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, also stains positive for desmin stain |
Leiomyosarcoma |
|
|
LH acts on theca cells to make ____ via _____ (enzyme). This product crosses over into granulosa cells where aromatase converts it to estradiol when activated by FSH |
Makes androstenedione from cholesterol via desmolase |
|
|
Diagnostic criteria for PCOS |
2 of the 3 - oligo/anovulation, hyperandrogenism, polycystic ovaries on ultrasound |
|
|
Increased LH/FSH ratio |
PCOS - LH stimulates theca cells to make androgens (that's why you get hirsutism) and that stimulates strogen production from granulosa cells (which feed back and inhbit FSH production) - that's why your ratio is greater (LH/FSH) |
|
|
Clomiphene mechansim of action |
Partial agonist at estrogen receptors in the hypothalamus and relatively decreases the negative feedback of estrogen, therefore increases FSH |
|
|
CA-125 |
marker for ovarian cancer, but not specific, so mainly used to monitor disease |
|
|
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 |
|
|
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 |
Brenner tumor |
|
|
What are the ovarian germ cell tumors? |
teratoma, dysgerminoma, endodermal sinus (yolk sac), and choriocarcinoma |
|
|
Teratoma in patients with hyperthyroid? |
Struma ovarii teratoma - can have functional thyroid tissue in it |
|
|
Ovarian tumor equavalent of seminoma in males. Made of undifferentiated germ cells - "sheets of uniform cells". May produce LDH and hCG and associated with Turners syndrome |
Dysgerminoma |
|
|
Elevated AFP, with schiller-duval bodies in ovaries (look like glomeruli) |
Yolk sac tumor aka endodermal sinus tumor |
|
|
What are the three types of stroma/sex cord ovarian tumors? |
Fibromas, granulosa-theca cell, sertoli-leydig cell |
|
|
Meig's syndrome |
Fibroma (benign ovarian tumor), ascities, and pleural effusion (hydorthorax) |
|
|
Call exner bodies - eosinophilic fluid-filled spaces between granulosa cells |
Granulosa cell tumor - malignant, make estrogen/progesterone/inhibin and can cause endometrial hyperplasia or percocious puberty |
|
|
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? |
In trisomy 18 - all are low. In 21, hCG is high |
|
|
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 |
|
|
edematous/grapelike chorionic villi are the buzzword for |
hydatiform mole pregnancy |
|
|
Complete vs partial hydatiform mole pregnancy |
complete is 46xx or 46xy and have a REALLY REALLY HIGH hCG. partial is 69xxy or xxx or xyy, not as high hCG, normal uterine size and 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. 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/abuse/smoking/cocaine increase risk of this happening |
|
|
What is HELLP syndrome? |
Hemolysis, Elevated Liver enzymes, and Low Platelets (anemic, jaundic, brusing, bleeding) and hypertension |
|
|
Pathogenesis of gestational diabetes? |
HPL - human placental lactogen - this is physiologically important because it decreases maternal insulin sensitivity 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 |
|
|
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) Hyertension, (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? |
(1) indomethicin (cox inhibitor preventing stimulatory PGE formation), (2) Nifedipine - calcium channel blocker causes myometrial relaxation, (3) Terbutaline - B2 agonist on uterus and relaxes myometrium, (4) Magnesium sulfate for seizure prophylaxis |
|
|
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 |
(1) Mifeprostone - synthetic steroid that's a competitive inhibitor of progesterone receptors - used for abortions in addition to (2) misoprostol - OGE analog (makes you contract) and (3) 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, 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 cancer, 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. It's 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 serious/bloody nipple discharge |
Intraductal papilloma |
|
|
Large benign bulky tumor of the breast with leaf like projections on histology |
Phyllodes tumor |
|
|
DCIS - ductal carcinoma in situ - what are the subtypes? |
(1) Comedocarcinoma - caseous necrosis, solid, cribiform, papillary, micropapillary |
|
|
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 + |
LCIS - lobular carcinoma in situ |
|
|
Firm, rock hard, immobile breast mass with sharp margins, often arises from DCIS |
Invasive ductal carcinoma |
|
|
Inactivation of E-cadherin genes, ER+ and PR+ breast cancer, and also has signet ring cells |
invasive lobular carcinoma |
|
|
Tamoxifen activity in breast tissue vs endometrial tissue? |
Antagonist at ER in breast, but 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 and inhibits production of estrogen - used in post menopausal women with breast cancer. Side effect - osteoperosis due to antagonistic effect on bones |
